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1.
Mol Biol Rep ; 50(4): 3413-3428, 2023 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-36754932

RESUMO

BACKGROUND: Y-box binding protein 1 (YBX1) is a multifunctional oncoprotein that can interact with several long non-coding RNAs (lncRNAs) to regulate metastasis in malignancies including breast cancer (BC). In the present study, we demonstrated the association of YBX1 with oncogenic lncRNA SBF2-AS1 (SET-binding factor 2 antisense RNA 1) via PI3K/AKT/mTOR signaling to regulate BC cell proliferation. We further explored the involvement of the YBX1/SBF2-AS1/PI3K/AKT/mTOR axis in the restoration of tamoxifen (TAM) sensitivity. METHODS AND RESULTS: YBX1-SBF2-AS1 association was predicted in silico and verified by RNA immunoprecipitation (RIP)-qPCR assay. Transfection experiments, Real-time RT PCR, Western blots, Phospho AKT/mTOR antibody array kit, and cell proliferation/apoptosis assays were employed to detect the YBX1/SBF2-AS1/ PI3K/AKT/mTOR axis and its effects upon TAM treatment in vitro. We identified that the YBX1 protein specifically binds to lncRNA SBF2-AS1. Our transfection experiments in MCF-7 and MDA-MB-468 cells with SBF2-AS1 silenced or overexpressed YBX1 plasmids, and their negative controls revealed that YBX1 regulates the expression of SBF2-AS1 by forming a positive feedback loop for its activation. We further demonstrated YBX1-SBF2-AS1 association exerts its effects on cell proliferation via PI3K/AKT/mTOR signaling pathway. Furthermore, we observed an increase in TAM sensitivity in BC cells after the knockdown of YBX1-SBF2-AS1 marked by decreased cell proliferation through disruption of the PI3K/AKT/mTOR axis. CONCLUSION: Our study has identified a novel YBX1/SBF2-AS1/PI3K/AKT/mTOR regulatory axis which may serve as a potential target to improve the effectiveness and efficacy of TAM treatment in BC.


Assuntos
Neoplasias da Mama , RNA Longo não Codificante , Humanos , Feminino , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Fosfatidilinositol 3-Quinases/genética , Fosfatidilinositol 3-Quinases/metabolismo , Tamoxifeno/farmacologia , Neoplasias da Mama/genética , Linhagem Celular Tumoral , Transdução de Sinais , Serina-Treonina Quinases TOR/genética , Serina-Treonina Quinases TOR/metabolismo , Proliferação de Células/genética , Regulação Neoplásica da Expressão Gênica , Proteína 1 de Ligação a Y-Box/genética , Proteína 1 de Ligação a Y-Box/metabolismo
2.
Mol Biol Rep ; 50(7): 6029-6037, 2023 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-37286777

RESUMO

BACKGROUND: Compared to other breast cancer subtypes, triple-negative breast cancer (TNBC) has always been challenging for clinicians due to its aggressive behavior and lack of a specific treatment. There is a confirmed association between invasive features of tumors and increased epithelial-mesenchymal transition (EMT) process, which is consistent with a higher rate of EMT in TNBC. METHODS AND RESULTS: We investigated the expression of EMT-related genes, SNAI1 and MMP7, and EMT-related lncRNAs, treRNA and SBF2-AS1, in 50 TNBC tumors and 50 non-TNBC tumors to reveal more regulators and effectors involved in TNBC malignancy. In the present study, we showed the overexpression of all the studied genes and lncRNAs in TNBC tumors compared to non-TNBC samples. Moreover, a significant association was observed between MMP7 and treRNA expression levels and larger tumor size. A positive correlation between SNAI1 and lncRNA treRNA expression levels was also detected. CONCLUSIONS: Due to the differential expression and the potential diagnostic power of the studied genes, SBF2-AS1 and treRNA can be proposed as new probable biomarkers and therapeutic targets in TNBC.


Assuntos
MicroRNAs , RNA Longo não Codificante , Neoplasias de Mama Triplo Negativas , Humanos , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo , Metaloproteinase 7 da Matriz/genética , Neoplasias de Mama Triplo Negativas/patologia , Regulação Neoplásica da Expressão Gênica/genética , Linhagem Celular Tumoral , Proliferação de Células/genética , MicroRNAs/genética , Transição Epitelial-Mesenquimal/genética
3.
World J Urol ; 40(6): 1561-1567, 2022 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-35428927

RESUMO

BACKGROUND: Extracorporeal shock wave lithotripsy (ESWL) is considered one of the best choices for the treatment of various kinds of urinary tract calculi, although it might cause acute kidney injury. OBJECTIVE: To measure the urinary long non-coding RNA-messenger RNA (LncRNA-mRNA) panel before and after ESWL to evaluate post-ESWL renal injury in a reliable and non-invasive method. PATIENTS AND METHODS: The study included 60 patients with renal stones treated with ESWL and 30 healthy volunteers. Voided urine samples were obtained before, 2 h, and 1 day after ESWL. We measured the urinary level of LncRNA (SBF2-AS1, FENDRR-19) and mRNA (GBP1, NLRP3) by real-time qPCR and compared the results with serum creatinine and eGFR. RESULTS: LncRNA (SBF2-AS1, FENDRR-19) and mRNA (GBP1, NLRP3) levels were higher in patients with renal stones when compared with healthy volunteers. They showed a statistically significant increase in the level of LncRNA-mRNA panel in baseline and after ESWL treatment. CONCLUSION: LncRNA (SBF2-AS1, FENDRR-19) and mRNA (GBP1, NLRP3) levels were significantly elevated following ESWL treatment, highlighting the usefulness of urinary biomarkers in identifying patients at higher risk of developing renal injury after ESWL treatment.


Assuntos
Cálculos Renais , Litotripsia , RNA Longo não Codificante , Injúria Renal Aguda/etiologia , Injúria Renal Aguda/urina , Biomarcadores/urina , Humanos , Rim/lesões , Rim/cirurgia , Cálculos Renais/etiologia , Cálculos Renais/terapia , Cálculos Renais/urina , Litotripsia/efeitos adversos , Proteína 3 que Contém Domínio de Pirina da Família NLR/urina , RNA Longo não Codificante/urina , RNA Mensageiro/urina
4.
Acta Med Okayama ; 76(6): 625-633, 2022 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-36549764

RESUMO

This investigation aimed to uncover the impact of a long noncoding RNA, SET-binding factor 2 antisense RNA1 (SBF2-AS1) on the malignant progression of gastric cancer (GC) and to further explore its underlying mechanism. SBF2-AS1 expression was quantified by qRT-PCR in GC cell lines and GC tissues. In vitro loss-of-function studies of SBF2-AS1, accompanied by flow cytometry, CCK-8, and cell invasion tests, were applied to elucidate the impact of SBF2-AS1 on the tumor progression of GC cells. Finally, Western blotting and a luciferase assay were used to detect WNT/LRP5 signaling pathway activation. SBF2-AS1 was aberrantly expressed in GC cell lines (p<0.05) and GC tissues (p<0.05). Cell invasive and proliferative capabilities were inhibited via SBF2-AS1 knockdown, resulting in apoptosis of NCI-N87 and MKN74 cells. Additionally, online database analysis uncovered a positive correlation between SBF2-AS1 and the Wnt/LRP5 signaling pathway (p<0.05). SBF2-AS1 knockdown blocked the Wnt/LRP5 signaling pathway, whereas the effects of SBF2-AS1 knockdown on the malignant genotype of MKN74 as well as NCI-N87 cells were partially restored by triggering the Wnt/ LRP5 signaling pathway. High expression of SBF2-AS1 was found in GC, the malignant progression of which was repressed via SBF2-AS1 knockdown by inhibiting the Wnt/LRP5 signaling pathway.


Assuntos
RNA Longo não Codificante , Neoplasias Gástricas , Via de Sinalização Wnt , Humanos , Carcinogênese , Linhagem Celular Tumoral , Proliferação de Células , Regulação Neoplásica da Expressão Gênica , Proteína-5 Relacionada a Receptor de Lipoproteína de Baixa Densidade/genética , Proteína-5 Relacionada a Receptor de Lipoproteína de Baixa Densidade/metabolismo , MicroRNAs/genética , RNA Longo não Codificante/metabolismo , Neoplasias Gástricas/genética , Neoplasias Gástricas/patologia , Via de Sinalização Wnt/genética
5.
Cancer Cell Int ; 21(1): 417, 2021 Aug 09.
Artigo em Inglês | MEDLINE | ID: mdl-34372871

RESUMO

Long non-coding RNAs refer to transcripts over 200 nt in length that lack the ability to encode proteins, which occupy the majority of the genome and play a crucial role in the occurrence and development of human diseases, especially cancers. SBF2-AS1, a newly identified long non-coding RNA, has been verified to be highly expressed in diversiform cancers, and is involved in processes promoting tumorigenesis, tumor progression and tumor metastasis. Moreover, upregulation of SBF2-AS1 expression was significantly related to disadvantageous clinicopathologic characteristics and indicated poor prognosis. In this review, we comprehensively summarize the up-to-date knowledge of the detailed mechanisms and underlying functions of SBF2-AS1 in diverse cancer types, highlighting the potential of SBF2-AS1 as a diagnostic and prognostic biomarker and even a therapeutic target.

6.
J Cell Mol Med ; 24(9): 5028-5038, 2020 05.
Artigo em Inglês | MEDLINE | ID: mdl-32301277

RESUMO

Evidence has indicated that M2 macrophages promote the progression of cancers, but few focus on the ability of M2 macrophage-derived exosomes in pancreatic cancer (PC). This study aims to explore how M2 macrophages affect malignant phenotypes of PC through regulating long non-coding RNA SET-binding factor 2 antisense RNA 1 (lncRNA SBF2-AS1)/microRNA-122-5p (miR-122-5p)/X-linked inhibitor of apoptosis protein (XIAP) axis. THP-1 cells were transformed into M1 macrophages by lipopolysaccharide and interferon-γ treatment, and into M2 macrophages after interleukin-4 treatment. The PANC-1 PC cell line with the largest lncRNA SBF2-AS1 expression was selected, and M2 macrophage-derived exosomes were isolated and identified. A number of assays were applied for the examination of lncRNA SBF2-AS1 expression, PC cell biological functions and subcellular localization of lncRNA SBF2-AS1. XIAP expression was detected, along with the interaction among lncRNA SBF2-AS1, miR-122-5p and XIAP. M2 macrophage exosomal lncRNA SBF2-AS1 expression's effects on the tumorigenic ability of PANC-1 cells in nude mice were also investigated. M2 macrophage-derived exosomes promoted progression of PC cells. Overexpressed lncRNA SBF2-AS1 promoted progression of PC cells. LncRNA SBF2-AS1 was found to act as a competing endogenous RNA to repress miR-122-5p and up-regulate XIAP. Constrained lncRNA SBF2-AS1 in M2 macrophage-derived exosomes contributed to restraining tumorigenic ability of PC cells. Collectively, our study reveals that constrained lncRNA SBF2-AS1 in M2 macrophage-derived exosomes increases miR-122-5p expression to restrain XIAP expression, which further inhibits PC progression.


Assuntos
Regulação Neoplásica da Expressão Gênica , Macrófagos/metabolismo , MicroRNAs/metabolismo , Oligonucleotídeos Antissenso/metabolismo , Neoplasias Pancreáticas/metabolismo , Proteínas Tirosina Fosfatases não Receptoras/metabolismo , RNA Longo não Codificante/metabolismo , Proteínas Inibidoras de Apoptose Ligadas ao Cromossomo X/metabolismo , Animais , Carcinogênese , Linhagem Celular Tumoral , Progressão da Doença , Exossomos/metabolismo , Feminino , Humanos , Hibridização in Situ Fluorescente , Proteínas Inibidoras de Apoptose/metabolismo , Lipopolissacarídeos/metabolismo , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Nus , Fenótipo , Transfecção
7.
J Cell Physiol ; 234(10): 18688-18696, 2019 08.
Artigo em Inglês | MEDLINE | ID: mdl-30912164

RESUMO

Evidence, demonstrating long noncoding RNAs (lncRNAs) as critical players in cancer, remains to increase. lncRNA SBF2-AS1 was reported to be involved in several cancers, such as hepatocellular carcinoma. However, the role of SBF2-AS1 in colorectal cancer (CRC) is unknown. We showed lncRNA SBF2-AS1 expression was growing in CRC samples, especially in advanced cases. Accordingly, SBF2-AS1 possesses higher expression in CRC cell lines than in normal cell line. Moreover, SBF2-AS1 high expression indicated a low survival rate. Functionally, SBF2-AS1 knockdown suppressed the proliferation, migration, and invasion of CRC cells. In terms of mechanism, SBF2-AS1 upregulation restrained the activity of miR-619-5p and led to overexpression of HDAC3. Importantly, downregulation of miR-619-5p or HDAC3 overexpression reversed SBF2-AS1-silencing-caused suppression on proliferation and metastasis. Summarily, our findings elucidated a crucial role of SBF2-AS1 as a miR-619-5p sponge, shedding novel light on lncRNA-related prognostics.


Assuntos
Neoplasias Colorretais/genética , Neoplasias Colorretais/patologia , Histona Desacetilases/metabolismo , MicroRNAs/metabolismo , RNA Longo não Codificante/metabolismo , Idoso , Animais , Sequência de Bases , Sítios de Ligação/genética , Linhagem Celular Tumoral , Movimento Celular/genética , Proliferação de Células/genética , Feminino , Regulação Neoplásica da Expressão Gênica , Inativação Gênica , Humanos , Masculino , Camundongos Endogâmicos BALB C , Camundongos Nus , MicroRNAs/genética , Invasividade Neoplásica , RNA Longo não Codificante/genética
8.
J Cell Biochem ; 120(9): 15422-15428, 2019 09.
Artigo em Inglês | MEDLINE | ID: mdl-31050364

RESUMO

The long noncoding RNAs (lncRNAs) SBF2 antisense RNA 1 (SBF2-AS1) was found to act as an oncogenic lncRNA in non-small-cell lung cancer (NSCLC), but the role of SBF2-AS1 in small-cell lung cancer (SCLC) was still unclear. The purpose of this study was to provide the clinical significance and biological function of SBF2-AS1 in SCLC. In our results, SBF2-AS1 was found to be upregulated in SCLC tissues compared with NSCLC tissues or adjacent normal lung tissues. Besides, SBF2-AS1 expression was also elevated in SCLC cell lines compared with the normal bronchial epithelial cell line or NSCLC lines. Moreover, high expression of SBF2-AS1 was associated with clinical stage, tumor size, lymph node metastasis and distant metastasis in SCLC patients. Survival analysis showed SCLC patients with high expression of SBF2-AS1 had shorter overall survival than patients with low expression of SBF2-AS1, and high expression of SBF2-AS1 acted as an independent poor prognostic factor for overall survival in SCLC patients. The study in vitro suggested inhibition of SBF2-AS1 obviously depressed cell proliferation, migration, and invasion in SCLC. In conclusion, SBF2-AS1 acts as a novel oncogenic lncRNA in SCLC.


Assuntos
Carcinoma Pulmonar de Células não Pequenas/patologia , Neoplasias Pulmonares/patologia , RNA Longo não Codificante/genética , Regulação para Cima , Células A549 , Carcinoma Pulmonar de Células não Pequenas/genética , Linhagem Celular Tumoral , Movimento Celular , Proliferação de Células , Progressão da Doença , Feminino , Regulação Neoplásica da Expressão Gênica , Humanos , Neoplasias Pulmonares/genética , Metástase Linfática , Masculino , Estadiamento de Neoplasias , Prognóstico , Análise de Sobrevida
9.
Biochem Biophys Res Commun ; 503(4): 2826-2832, 2018 09 18.
Artigo em Inglês | MEDLINE | ID: mdl-30115383

RESUMO

A growing number of studies has suggested that long non-coding RNAs (lncRNAs) exert essential roles in the development and progression of hepatocellular carcinoma (HCC). However, the roles of lncRNA and its molecular mechanism in HCC are largely unknown. In the present study, the functions and molecular mechanisms of a novel lncRNA, SET-binding factor 2 (SBF2) antisense RNA1 (SBF2-AS1), were investigated in HCC tissues and cell lines. We found that the expression levels of SBF2-AS1 were significantly up-regulated in HCC tissues and correlated with poor prognosis. SBF2-AS1 knockdown could inhibit the proliferation of HCC cells and attenuate the development of HCC tumor in vivo. Moreover, wound healing and Transwell assays revealed that down-regulation of SBF2-AS1 suppressed the migration and invasion of HCC cells by modulating epithelial-mesenchymal transition (EMT) ability. Mechanistically, we observed that SBF2-AS1 served as a competing endogenous RNA (ceRNA) of miR-140-5p. Subsequently, transforming growth factor beta receptor 1 (TGFBR1) was certified as a direct target of miR-140-5p and enforcing SBF2-AS1 expression elevated TGFBR1 expression in HCC. Taken together, our study suggested that SBF2-AS1 modulated TGFBR1 through sponging miR-140-5p in HCC development and progression indicating that SBF2-AS1 might be further chosen as a potential anticancer therapeutic target and a promising prognostic biomarker for HCC.


Assuntos
Carcinoma Hepatocelular/genética , Regulação Neoplásica da Expressão Gênica , Neoplasias Hepáticas/genética , MicroRNAs/genética , RNA Longo não Codificante/genética , Receptor do Fator de Crescimento Transformador beta Tipo I/genética , Animais , Carcinoma Hepatocelular/metabolismo , Carcinoma Hepatocelular/mortalidade , Carcinoma Hepatocelular/patologia , Linhagem Celular Tumoral , Movimento Celular , Proliferação de Células , Progressão da Doença , Transição Epitelial-Mesenquimal/genética , Genes Reporter , Células Hep G2 , Humanos , Neoplasias Hepáticas/metabolismo , Neoplasias Hepáticas/mortalidade , Neoplasias Hepáticas/patologia , Luciferases/genética , Luciferases/metabolismo , Masculino , Camundongos , Camundongos Nus , MicroRNAs/metabolismo , Oligorribonucleotídeos/genética , Oligorribonucleotídeos/metabolismo , Prognóstico , RNA Longo não Codificante/antagonistas & inibidores , RNA Longo não Codificante/metabolismo , Receptor do Fator de Crescimento Transformador beta Tipo I/metabolismo , Transdução de Sinais , Análise de Sobrevida , Ensaios Antitumorais Modelo de Xenoenxerto
10.
Urolithiasis ; 52(1): 113, 2024 Aug 06.
Artigo em Inglês | MEDLINE | ID: mdl-39105900

RESUMO

Long non-coding ribose nucleic acids (lncRNAs) have been implicated in the development of nephrolithiasis. The study aims to investigate the interplay of lncRNA SBF2-AS1 (SETbinding factor 2 antisense RNA 1) and NLR family pyrin domain containing 3 (NLRP3) in regulating the calcium oxalate monohydrate (COM)-induced human kidney HK-2 cell injury. HK-2 cells were treated with COM (100 µg/mL) to create a cellular model of kidney injury. Gene and protein expression was assessed by quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR) and Western blot. Proliferation and apoptosis rates, as well as levels of malondialdehyde (MDA), lactate dehydrogenase (LDH), superoxide dismutase (SOD), tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, and IL-6 were measured. Additionally, potential miRNAs interacting with SBF2-AS1 and NLRP3 were predicted utilizing the starBase and TargetScan databases. The interference of SBF2-AS1 resulted in increased cell proliferation and SOD levels in HK-2 cells after COM induction. SBF2-AS1 silencing also reduced COM-induced cell death and inflammatory cytokine production by down-regulating NLRP3 protein expression. Conversely, forced upregulation of NLRP3 abrogated the effect of SBF2-AS1 interference. Notably, SBF2-AS1 interference on COM-induced oxidative stress and COM-induced cellular damage was rescued by antioxidant, indicating the involvement of oxidative burden in COM-induced damage. miR-302e acted as a mediator miRNA linking the functional association of SBF2-AS1 and NLRP3. Silencing SBF2-AS1 promoted miR-302e level and miR-302e reduced NLRP3 expression in HK-2 cells to protect against COM-induced damage. In summary, these findings suggest that downregulation of lncRNA SBF2-AS1 can potentially protect HK-2 cells from COM-induced injury by modulating the miR-302e/NLRP3 pathway.


Assuntos
Oxalato de Cálcio , MicroRNAs , Proteína 3 que Contém Domínio de Pirina da Família NLR , RNA Longo não Codificante , Humanos , Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo , Proteína 3 que Contém Domínio de Pirina da Família NLR/genética , MicroRNAs/metabolismo , MicroRNAs/genética , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo , Oxalato de Cálcio/metabolismo , Transdução de Sinais/efeitos dos fármacos , Linhagem Celular , Proliferação de Células/genética , Proliferação de Células/efeitos dos fármacos , Apoptose/efeitos dos fármacos , Apoptose/genética , Técnicas de Silenciamento de Genes , Estresse Oxidativo/efeitos dos fármacos
11.
Kaohsiung J Med Sci ; 38(4): 302-311, 2022 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-34850542

RESUMO

Long noncoding RNA SET-binding factor 2 (SBF2) antisense RNA 1 (AS1) is associated with the growth and metastasis of multiple cancer types, but its biological roles in serous ovarian carcinoma (SOC) remain unclear. In this study, the aberrant upregulation of SBF2-AS1 is detected in SOC after analysis of differentially expressed genes between SOC tissues and normal fallopian tubes from the public Gene Expression Omnibus (GEO) database. We determine that knockdown of SBF2-AS1 inhibits SOC cell proliferation and invasion by sponging miR-338-3p. MiR-338-3p acts as a tumor suppressor in SOC, and E26 transformation specific-1 (ETS1) is identified as a potential target of miR-338-3p regulation. Furthermore, SBF2-AS1 could modulate ETS1 by operating as a competing endogenous RNA for miR-338-3p. This finding elucidates a new mechanism for SBF2-AS1 in SOC development and provides a potential target for SOC therapeutic intervention.


Assuntos
Proliferação de Células , MicroRNAs , Neoplasias Ovarianas , RNA Longo não Codificante , Linhagem Celular Tumoral , Movimento Celular/genética , Proliferação de Células/genética , Feminino , Regulação Neoplásica da Expressão Gênica , Humanos , MicroRNAs/genética , MicroRNAs/metabolismo , Neoplasias Ovarianas/genética , RNA Antissenso/genética , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo
12.
Curr Pharm Des ; 28(18): 1513-1522, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35440300

RESUMO

Long non-coding RNA (lncRNA) is a new kind of RNA with a length of over 200 nucleotides. Current frontiers revealed that lncRNAs implicate in various tumor progression, including tumorigenesis, proliferation, migration, invasion, metastasis, and angiogenesis. Recently discovered long non-coding RNA SETbinding factor 2 antisense RNA 1 (lncRNA SBF2-AS1), an oncogenic antisense RNA to SBF2, locates at 11p15.1 locus and is 2708 nt long. Accumulating evidence has demonstrated that lncRNA SBF2-AS1 participates in the progression of the various tumor, including pathogenesis, diagnosis, treatment, and prognosis of acute myeloid leukemia (AML), breast cancer (BC), cervical cancer (CC), clear cell renal cell carcinoma (ccRCC), colorectal cancer (CRC), diffuse large B-cell lymphoma (DLBCL), esophageal squamous cell carcinoma (ESCC), gastric cancer (GC), glioma, glioblastoma (GBM), hepatocellular carcinoma (HCC), lung cancer (LC), lung adenocarcinoma (LUAD), non-small cell lung cancer (NSCLC), osteosarcoma (OS), pancreatic cancer (PC), papillary thyroid cancer (PTC), small cell lung cancer (SCLC). Therefore, we summarized the underlying mechanisms of lncRNA SBF2-AS1 in various cancers to utilize its therapeutic function in target-selective treatment modalities.


Assuntos
Carcinoma Hepatocelular , Carcinoma Pulmonar de Células não Pequenas , Neoplasias Esofágicas , Carcinoma de Células Escamosas do Esôfago , Neoplasias Hepáticas , Neoplasias Pulmonares , MicroRNAs , RNA Longo não Codificante , Carcinogênese/genética , Carcinoma Hepatocelular/genética , Carcinoma Pulmonar de Células não Pequenas/genética , Linhagem Celular Tumoral , Movimento Celular/genética , Proliferação de Células/genética , Carcinoma de Células Escamosas do Esôfago/genética , Regulação Neoplásica da Expressão Gênica , Humanos , Neoplasias Hepáticas/genética , Neoplasias Pulmonares/patologia , MicroRNAs/genética , RNA Antissenso , RNA Longo não Codificante/genética
13.
Aging (Albany NY) ; 13(15): 19260-19271, 2021 08 02.
Artigo em Inglês | MEDLINE | ID: mdl-34341185

RESUMO

SBF2-AS1 is an oncogenic long non-coding RNA (lncRNA). However, its role and mechanism in hepatocellular carcinoma (HCC) is still not completely clear. The HepG2, Hep3B, Bel-7402 and HL-7702 cell lines were used in our experiments. The CCK-8 kit and EdU staining were applied to detect cell viability and multiplication. The wound healing and Boyden chamber cell migration assays were employed to test the migration ability of cells. The levels of TGF-ß1 mRNA, lncRNA SBF2-AS1, and miR-361-5p were assessed by real-time PCR. TGF-ß1 protein levels were evaluated by western blotting. The direct interaction between miR-361-5p and TGF-ß1 was determined by luciferase reporter assays. A xenograft mouse model (XMM) was established to comprehensively study the effect and mechanisms of lncRNA SBF2-AS1. lncRNA SBF2-AS1 concentration in HCC cells exceeded that in a normal hepatocyte cell line. The downregulation of lncRNA SBF2-AS1 upregulated miR-361-5p levels in HCC cells. And, miR-361-5p negatively regulate TGF-ß1 expression in HCC cells. The suppression of miR-361-5p attenuated the influence of lncRNA SBF2-AS1 downregulation on the viability, proliferation, and migration capability of HCC cells. Further, the downregulation of lncRNA SBF2-AS1 inhibited neoplasm growth in an XMM of HCC. Simultaneously, miR-361-5p was upregulated and TGF-ß1 was downregulated after lncRNA SBF2-AS1 knocked down. In conclusion, downregulation of lncRNA SBF2-AS1 inhibits HCC proliferation and migration through the regulation of the miR-361-5p/TGF-ß1 signaling pathway.


Assuntos
Carcinoma Hepatocelular/genética , Regulação Neoplásica da Expressão Gênica , Neoplasias Hepáticas/genética , MicroRNAs/genética , RNA Longo não Codificante/genética , Fator de Crescimento Transformador beta1/genética , Animais , Carcinogênese/genética , Carcinogênese/metabolismo , Carcinoma Hepatocelular/metabolismo , Carcinoma Hepatocelular/patologia , Linhagem Celular Tumoral , Movimento Celular/genética , Proliferação de Células/genética , Progressão da Doença , Humanos , Neoplasias Hepáticas/metabolismo , Neoplasias Hepáticas/patologia , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Nus , MicroRNAs/metabolismo , RNA Longo não Codificante/metabolismo , Transdução de Sinais , Análise de Sobrevida , Fator de Crescimento Transformador beta1/metabolismo , Ensaios Antitumorais Modelo de Xenoenxerto
14.
Technol Cancer Res Treat ; 20: 15330338211011966, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34159865

RESUMO

LncRNA SET-binding factor 2 (SBF2) antisense RNA1 (SBF2-AS1) has been proven to play an oncogenic role in various types of tumors, but the prognostic role of SBF2-AS1 in tumors, especially in diffuse lower-grade glioma (LGG), is still unclear. Here, we aimed to investigate the prognostic value of SBF2-AS1 in LGG. The LGG expression profiles from The Cancer Genome Atlas (TCGA, n = 524) and Chinese Glioma Genome Atlas (CGGA, n = 431) were mined by Kaplan-Meier analysis, Cox regression analysis, Chi-square test and GSEA analysis. Through Kaplan-Meier analysis, we found the prognosis of LGG patients with high expression of SBF2-AS1 were worse than that of patients with low expression (Log Rank P < 0.001). Cox analysis showed SBF2-AS1 was an independent prognostic factor for poorer overall survival in LGG (P < 0.05). SBF2-AS1 was found to be significantly related to IDH mutation status and SBF2-AS1 was highly expressed in IDH wildtype group. GSEA analysis obtained a total of 126 GO terms and 6 KEGG pathways that were significantly enriched in SBF2-AS1 high expression phenotype (NOM P value < 0.05). We found these 126 GO terms and KEGG pathways were mainly related to immunity. In conclusion, lncRNA SBF2-AS1 expression is an immune-related lncRNA associated with unfavorable overall survival in LGG. SBF2-AS1 could be a reliable prognostic biomarker for patients with LGG.


Assuntos
Neoplasias do Sistema Nervoso Central/genética , Neoplasias do Sistema Nervoso Central/patologia , Glioma/genética , Glioma/patologia , RNA Longo não Codificante/genética , Adulto , Biomarcadores Tumorais/genética , Bases de Dados Genéticas , Feminino , Expressão Gênica , Humanos , Imunidade/genética , Isocitrato Desidrogenase/genética , Estimativa de Kaplan-Meier , Masculino , Mutação , Gradação de Tumores , Prognóstico , Modelos de Riscos Proporcionais , Taxa de Sobrevida
15.
Technol Cancer Res Treat ; 20: 15330338211004915, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33906548

RESUMO

BACKGROUND: The mortality and recurrence of patients with cancer is of high prevalence. SET-binding factor 2 (SBF2) antisense RNA1 (lncRNA-SBF2-AS1) is a promising long non-coding RNA. There is increasing evidence that SBF2-AS1 is abnormally expressed in various tumors and is associated with cancer prognosis. However, the identification of the effect of lncRNA SBF2-AS1 in tumors remains necessary. MATERIALS AND METHODS: Up to November 2, 2020, electronic databases, including PubMed, Cochrane Library, EMBASE, Medline, and Web of Science, were searched. The results were evaluated by pooled odds ratios (ORs) and hazard ratios (HRs) with 95% confidence intervals (CIs). RESULTS: A total of 11 literatures on cancer patients were included for the present meta-analysis. The combined results revealed that high expression of SBF2-AS1 was significantly associated with unfavorable overall survival (OS) (HR = 1.48, 95% CI: 1.34-1.62, P < 0.00001) in a variety of cancers. In additional, the increase in SBF2-AS1 expression was also correlated with tumor size ((larger vs. smaller) OR = 2.34, 95% CI: 1.47-3.70, P = 0.0003), advanced TNM stage ((III/IV vs. I/II) OR = 2.78, 95% CI: 1.75-4.41, P < 0.0001), lymph node metastasis ((Positive vs. Negative) OR = 3.06, 95% CI: 1.93-4.86, P < 0.00001), and histological grade ((poorly vs. well/moderately) OR = 2.58, 95% CI: 1.47-4.52, P = 0.001) in patients with cancer. Furthermore, The Cancer Genome Atlas (TCGA) dataset valuated that SBF2-AS1 was upregulated in a variety of tumors, and predicted the worse prognosis. CONCLUSIONS: Our results of this meta-analysis demonstrate that high SBF2-AS1 expression may become a potential target for predicting the prognosis of human cancers.


Assuntos
Biomarcadores Tumorais/genética , Neoplasias/patologia , RNA Longo não Codificante/genética , Regulação Neoplásica da Expressão Gênica , Humanos , Neoplasias/genética , Prognóstico , Taxa de Sobrevida
16.
Cancer Manag Res ; 13: 571-578, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33519236

RESUMO

PURPOSE: Currently, there is no efficient and feasible method for diffuse large B-cell lymphoma (DLBCL) in clinical practice, and the main reason is the unclear pathogenesis of DLBCL, which leads to a high fatality rate of DLBCL. METHODS: Therefore, it is meaningful to explore the molecular mechanism of DLBCL and find a targeted therapeutic approach from the molecular level. RESULTS: Long non-coding RNA (lncRNA) SBF2-AS1 was highly expressed in DLBCL tissues and cell lines. Silencing of SBF2-AS1 inhibited the viability and growth of OCI-LY-3 cells. Furthermore, SBF2-AS1 acted as a sponge of miR-494-3p and inhibited its expression. And miR-494-3p directly targeted FGFR2. Functionally, forced expression of miR-494-3p or knockdown of FGFR2 removed the promoted effects of lncRNA SBF2-AS1 on DLBCL development. In vivo tumorigenesis experiments indicated SBF2-AS1 accelerated tumor growth via miR-494-3p/FGFR2 axis. CONCLUSION: Our study revealed that SBF2-AS1 promoted the growth of DLBCL, which were mediated by miR-494-3p/FGFR2 axis.

17.
Biol Open ; 2020 Mar 30.
Artigo em Inglês | MEDLINE | ID: mdl-32229486

RESUMO

Esophageal squamous cell carcinoma (ESCC) is an intractable esophageal cancer caused by smoking, alcohol consumption and nutritional deficiencies. Recently, long non-coding RNA SET-binding factor 2 antisense RNA 1 (SBF2-AS1) was validated as an oncogene in multiple cancers. However, the mechanism of SBF2-AS1 in ESCC progression is poorly understood. In the present research, we found that the expression of SBF2-AS1 and PFN2 was up-regulated, while miR-494 was down-regulated in ESCC tumors and cells using quantitative real-time polymerase chain reaction (qRT-PCR). 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay and transwell assay demonstrated that silencing of SBF2-AS1 suppressed proliferation, migration and invasion. Moreover, western blot showed that SBF2-AS1 deletion also inhibited epithelial to mesenchymal transition (EMT) by detecting MMP9, Vimentin and E-cadherin protein expression. We confirmed that miR-494 was a target of SBF2-AS1 by luciferase reporter system, RIP and RNA pull-down assay. In addition, miR-494 inhibitor reversed the repression induced by SBF2-AS1 silencing on ESCC cell proliferation, migration, invasion and EMT. Furthermore, PFN2 was negatively regulated by miR-494. Besides, restoration of PFN2 inversed the inhibition effects on cell proliferation, migration, invasion and EMT induced by SBF2-AS1 silencing in ESCC. In conclusion, SBF2-AS1 contributed to cell proliferation, migration, invasion and EMT in ESCC by enhancing PFN2 expression via sponging miR-494, providing promising biomarkers for ESCC diagnosis and treatment.

18.
Kaohsiung J Med Sci ; 36(10): 808-816, 2020 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-32602632

RESUMO

Papillary thyroid cancer (PTC) is a frequent thyroid malignancy. With the significant regulatory role in tumor progression, more attention has been employed to investigate mechanism of long noncoding RNAs (lncRNAs) in progression of PTC. We prospectively explored the mechanism whereby lncRNA SET-binding factor 2-antisense RNA1 (SBF2-AS1) is implicated in pathogenesis of PTC. First, differentially expressed SBF2-AS1 between PTC and normal adjacent thyroid tissues was determined, and result indicated a higher SBF2-AS1 expression in PTC tissues than adjacent normal tissues. Moreover, highly SBF2-AS1 expression predicted a poor prognosis in PTC patients. Second, SBF2-AS1 overexpression promoted cell viability and cycle of PTC, while inhibited cell apoptosis. However, SBF2-AS1 downregulation reduced viability and cycle, while promoted cell apoptosis. Moreover, SBF2-AS1 could bind with miR-431-5p and showed negative correlation with miR-431-5p in PTC patients. Furthermore, miR-431-5p bind with cyclin-dependent kinase (CDK) 14 and showed negative correlation with CDK14 in PTC patients. Finally, overexpression of CDK14 counteracted with the inhibitory role of SBF2-AS1 downregulation on cell viability, cycle, and apoptosis of PTC. In conclusion, SBF2-AS1 exhibited oncogenic property in PTC, and knockdown of SBF2-AS1 could be a therapeutic strategy for PTC.


Assuntos
MicroRNAs/metabolismo , RNA Bacteriano/metabolismo , RNA Longo não Codificante/metabolismo , Câncer Papilífero da Tireoide/metabolismo , Western Blotting , Linhagem Celular Tumoral , Proliferação de Células/genética , Proliferação de Células/fisiologia , Citometria de Fluxo , Regulação Neoplásica da Expressão Gênica/genética , Regulação Neoplásica da Expressão Gênica/fisiologia , Humanos , Técnicas In Vitro , MicroRNAs/genética , RNA Bacteriano/genética , RNA Longo não Codificante/genética , Transdução de Sinais/genética , Transdução de Sinais/fisiologia , Câncer Papilífero da Tireoide/genética
19.
Aging (Albany NY) ; 12(18): 17902-17920, 2020 Sep 25.
Artigo em Inglês | MEDLINE | ID: mdl-32976115

RESUMO

Non-small cell lung cancer (NSCLC) is a type of refractory malignant lung cancer with a high rate of metastasis and mortality. Currently, long non-coding RNA (lncRNA) SBF2 Antisense RNA 1 (SBF2-AS1) is considered as a biomarker for a variety of tumors. However, the function of SBF2-AS1 in the growth and metastasis of NSCLC needs to be further studied. In this study, we revealed that SBF2-AS1 was overexpressed in NSCLC tissues compared with that in normal tissues. SBF2-AS1 silencing restrained the growth and aggressive phenotypes of NSCLC cell in vitro. Consistently, SBF2-AS1 knockdown hindered the growth of NSCLC cell in nude mice. The following luciferase reporter gene assay and RNA immunoprecipitation (RIP) assay suggested the relationship between miR-338-3p and SBF2-AS1. The rescue experiments showed that miR-338-3p inhibitor abolished SBF2-AS1 silencing caused inhibition on the growth, migration and invasiveness of NSCLC cell. The luciferase reporter assay and immunoblotting assay validated that A Disintegrin and Metalloprotease 17 (ADAM17) was a target of miR-338-3p. In addition, SBF2-AS1 positively regulated the level of ADAM17 through sponging for miR-338-3p. Finally, we revealed that SBF2-AS1 contributed to the proliferation and metastatic phenotypes of NSCLC cell via regulating miR-338-3p/ADAM17 axis.

20.
DNA Cell Biol ; 39(7): 1290-1298, 2020 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-32364763

RESUMO

Long noncoding RNA SBF2 antisense RNA 1 (lncRNA SBF2-AS1) has been reported to be involved in non-small-cell lung cancer (NSCLC) tumorigenesis. However, the biological role and regulatory mechanism of lncRNA SBF2-AS1 on NSCLC metastasis remain largely unknown. In this study, the expression level and functional role of SBF2-AS1 were investigated in both NSCLC tissues and cell lines. We found that SBF2-AS1 was upregulated in both NSCLC tissues and cell lines. Patients with high levels of SBF2-AS1 have larger tumors, higher malignancy, and poor prognosis. Knockdown of SBF2-AS1 significantly inhibited tumor growth in vivo and cell proliferation, migration, and invasion in vitro. Moreover, bioinformatics analysis, chromatin immunoprecipitation assay, and luciferase reporter assay proved that the upregulation of SBF2-AS1 was mediated by transcription factor E2F1. Further experiments demonstrated that miR-362-3p had complementary binding site with 3'-UTR of SBF2-AS1. Besides, luciferase reporter assay validated that GRB2 was the target protein of miR-362-3p. Rescue experiments showed that SBF2-AS1 silencing inhibited cell invasion and migration, while cotransfection si-SBF2-AS1 and miR-362-3p inhibitor rescued the effect of si-SBF2-AS1. These results demonstrate that E2F1-induced overexpression of SBF2-AS1 promotes the expression of GRB2 by targeting miR-362-3p to facilitate the metastasis of NSCLC.


Assuntos
Carcinoma Pulmonar de Células não Pequenas/patologia , Fator de Transcrição E2F1/metabolismo , Proteína Adaptadora GRB2/genética , Regulação Neoplásica da Expressão Gênica/genética , Neoplasias Pulmonares/patologia , MicroRNAs/genética , RNA Longo não Codificante/genética , Regiões 3' não Traduzidas/genética , Células A549 , Sequência de Bases , Carcinogênese/genética , Carcinoma Pulmonar de Células não Pequenas/genética , Movimento Celular/genética , Proliferação de Células/genética , Humanos , Neoplasias Pulmonares/genética , Invasividade Neoplásica/genética , Metástase Neoplásica/genética , Regulação para Cima/genética
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