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BACKGROUND: Multiple studies have revealed that long non-coding RNA (lncRNA) NR2F2-AS1 plays a role in affecting cancer cell proliferation and metastasis. Here, both in vitro and in vivo experiments were performed for investigating the function and mechanism of NR2F2-AS1 in human osteosarcoma (OS). METHODS: The NR2F2-AS1 level in human OS tissues and adjacent non-tumor tissues was examined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The NR2F2-AS1 overexpression model was constructed in OS cells, then cell proliferation, invasion, and apoptosis were monitored. The OS xenograft model was established in nude mice using NR2F2-AS1-overexpressed OS cells. The downstream target genes of NR2F2-AS1 were predicted. qRT-PCR and Western blot were implemented to validate the profiles of miR-425-5p and HMGB2. The targeting link between NR2F2-AS1 and miR-425-5p, miR-425-5p and HMGB2 was further probed by dual-luciferase reporter experiment. RESULTS: In comparison to adjacent non-tumor tissues, OS tissues showed upregulated NR2F2-AS1 expression. Higher NR2F2-AS1 level was predominantly correlated with worse clinical stages. In vivo and in vitro tests corroborated that NR2F2-AS1 overexpression spurred OS cell proliferation, growth, invasion, and choked apoptosis. Mechanistically, NR2F2-AS1 hampered miR-425-5p expression as its competitive endogenous RNA (ceRNA). Thus, NR2F2-AS1 facilitated the HMGB2 expression. However, miR-425-5p inhibited HMGB2 expression by targeting the latter. CONCLUSION: NR2F2-AS1 expedited the evolution of OS by elevating HMGB2 levels through sponging miR-425-5p. The NR2F2-AS1/miR-425-5p/HMGB2 regulatory axis is a promising target in treating human OS.
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Neoplasias Ósseas , Proteína HMGB2 , MicroRNAs , Osteossarcoma , RNA Longo não Codificante , Animais , Humanos , Camundongos , Neoplasias Ósseas/patologia , Linhagem Celular Tumoral , Movimento Celular/genética , Proliferação de Células/genética , Fator II de Transcrição COUP/genética , Fator II de Transcrição COUP/metabolismo , Regulação Neoplásica da Expressão Gênica/genética , Proteína HMGB2/genética , Proteína HMGB2/metabolismo , Camundongos Nus , MicroRNAs/genética , MicroRNAs/metabolismo , Osteossarcoma/genética , Osteossarcoma/patologia , RNA Longo não Codificante/genética , Fatores de Transcrição/genéticaRESUMO
Increasing numbers of miRNAs have been observed as oncogenes or tumor suppressors in colorectal cancer (CRC). It was recently reported that hsa-miR-106b-5p (miR-106b) promoted CRC cell migration and invasion. However, there were also studies showing contradictory results. Therefore, in the present study, we further explore the role of miR-106b and its downstream networks in the carcinogenesis of CRC. We observed that the expression of miR-106b is significantly increased in Pan-Cancer and CRC tissues compared with normal tissues from The Cancer Genome Atlas (TCGA) database. Furthermore, we used Transwell, Cell Counting Kit-8, and colony formation assays to clarify that miR-106b promotes the migratory, invasive, and proliferative abilities of CRC cells. For the first time, we systematically screened the target mRNAs and lncRNAs of miR-106b using TCGA database and the bioinformatics algorithms. Dual-luciferase reporter assay confirmed that NR2F2-AS1 and PLEKHO2 are the direct targets of miR-106b. Furthermore, NR2F2-AS1 acts as a competing endogenous RNA (ceRNA) to regulate PLEKHO2 expression by sponging miR-106b. The results of Gene set enrichment analysis (GSEA) and Western blot indicated that they play important roles in CRC progression by regulating MAPK pathway. Thus, miR-106b/NR2F2-AS1/PLEKHO2/MAPK signaling axis may suggest the potential usage in CRC treatment.
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Fator II de Transcrição COUP/genética , Carcinogênese/genética , Neoplasias Colorretais/genética , Peptídeos e Proteínas de Sinalização Intercelular/genética , MicroRNAs/genética , RNA Longo não Codificante/genética , Atlas como Assunto , Sequência de Bases , Sítios de Ligação , Fator II de Transcrição COUP/metabolismo , Carcinogênese/metabolismo , Carcinogênese/patologia , Linhagem Celular Tumoral , Movimento Celular , Proliferação de Células , Neoplasias Colorretais/metabolismo , Neoplasias Colorretais/patologia , Bases de Dados Genéticas , Regulação Neoplásica da Expressão Gênica , Genes Reporter , Células HCT116 , Humanos , Peptídeos e Proteínas de Sinalização Intercelular/metabolismo , Luciferases/genética , Luciferases/metabolismo , Sistema de Sinalização das MAP Quinases , MicroRNAs/metabolismo , RNA Longo não Codificante/metabolismoRESUMO
We in this study investigated the role of lncRNA NR2F2-AS1 in prostate carcinoma (PC). We showed that NR2F2-AS1 was upregulated in PC and positively correlated with CDK4. In PC cells, NR2F2-AS1 overexpression led to upregulated, while NR2F2-AS1 siRNA silencing led to downregulated CDK4. Follow-up study revealed that high levels of NR2F2-AS1 and CDK4 in PC tissues were closely correlated with the poor survival of PC patients. Cell proliferation data showed that NR2F2-AS1 overexpression led to increased, while NR2F2-AS1 siRNA silencing led to proliferation rate of PC cells. Moreover, NR2F2-AS1 also showed positive effects on cell cycle progression. In addition, CDK4 overexpression reduced the effects of NR2F2-AS1 siRNA silencing. Therefore, NR2F2-AS1 positively regulates CDK4 to promote cancer cell proliferation in PC.
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Carcinoma , RNA Longo não Codificante , Fator II de Transcrição COUP/genética , Linhagem Celular Tumoral , Proliferação de Células , Quinase 4 Dependente de Ciclina/genética , Seguimentos , Regulação Neoplásica da Expressão Gênica , Humanos , Masculino , Próstata , RNA Longo não Codificante/genéticaRESUMO
AIMS: Long non-coding RNA (lncRNA) NR2F2 antisense RNA 1 (NR2F2-AS1) is an oncogenic lncRNA in lung cancer. This study aimed to investigate the role of NR2F2-AS1 in colorectal cancer (CRC). METHODS: Tissue specimens were obtained from 63 CRC patients, and gene expression was analyzed by qPCR and western blot. Overexpression was performed to analyze gene interactions. A 5-year follow-up was carried out to perform survival analysis. Cell cycle progression and proliferation were analyzed by cell cycle assay and CCK-8 assay, respectively. RESULTS: We found that NR2F2-AS1 and cyclin-dependent kinase 6 (CDK6) were both upregulated in CRC and were positively correlated. NR2F2-AS1 siRNA silencing led to downregulated CDK6 and induced Gap 1 (G1) arrest of CRC cells. CDK6 overexpression rescued G1 arrest caused by NR2F2-AS1 siRNA silencing. High expression levels of NR2F2-AS1 were closely correlated with low overall 5-year survival rate. NR2F2-AS1 siRNA silencing led to decreased rate of CRC cell proliferation. CDK6 overexpression attenuated the effects of NR2F2-AS1 siRNA silencing on cancer cell proliferation. CONCLUSIONS: Downregulation of NR2F2-AS1 induces G1 arrest of CRC cells by downregulating CDK6.
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Neoplasias Colorretais/genética , Quinase 6 Dependente de Ciclina/genética , Pontos de Checagem da Fase G1 do Ciclo Celular/genética , RNA Longo não Codificante/genética , Adulto , Idoso , Western Blotting , Neoplasias Colorretais/metabolismo , Quinase 6 Dependente de Ciclina/metabolismo , Regulação para Baixo , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , RNA Antissenso/genética , RNA Antissenso/metabolismo , RNA Longo não Codificante/metabolismo , RNA Interferente Pequeno , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Regulação para CimaRESUMO
Recently, long noncoding RNAs (lncRNAs) are attracting wide attention in the field of cancer research because of its important role in cancer diagnosis and prognosis. But studies on the biological effects and relevant mechanisms of lncRNAs in non-small cell lung cancer (NSCLC) remain few and need to be enriched. Our study discussed the expression and biological effects of LncRNA NR2F2-AS1, and further explored its possible molecular mechanisms. As a result, elevated expression of NR2F2-AS1 was detected in NSCLC tissues and cells and was remarkably associated with the tumor, node, metastasis (TNM) stage and the status of lymphatic metastasis of patients. Down-regulated NR2F2-AS1 contributed to the promotion of cell apoptosis and the inhibition of cell proliferation and invasion in A549 and SPC-A-1 cells in vivo and vitro. Through bioinformatics analysis, NR2F2-AS1 functions as a ceRNA directly binding to miR-320b, BMI1 was a direct target of miR-320b. Combined with the following cellular experiments, the data showed that NR2F2-AS1 may influence the NSCLC cell proliferation, invasion and apoptosis through regulating miR-320b targeting BMI1.
Assuntos
Fator II de Transcrição COUP/genética , Carcinogênese/genética , Carcinoma Pulmonar de Células não Pequenas/genética , Neoplasias Pulmonares/genética , MicroRNAs/genética , Complexo Repressor Polycomb 1/genética , RNA Longo não Codificante/genética , Células A549 , Apoptose/genética , Carcinogênese/patologia , Carcinoma Pulmonar de Células não Pequenas/patologia , Linhagem Celular Tumoral , Movimento Celular/genética , Proliferação de Células/genética , Regulação para Baixo/genética , Regulação Neoplásica da Expressão Gênica/genética , Humanos , Neoplasias Pulmonares/patologia , Metástase Linfática/genética , Metástase Linfática/patologia , Prognóstico , Regulação para Cima/genéticaRESUMO
AIM: This study aims to investigate the potential role of lncRNA NR2F2-AS1 in the development of gastric cancer by affecting the levels of miR-320b and BMI1. BACKGROUND: Gastric cancer is a high-mortality malignancy, and understanding the underlying molecular mechanisms is crucial. Non-coding RNAs play an important role in gene expression, and their dysregulation can lead to tumor initiation and progression. OBJECTIVE: This study aims to determine the pathological role of LncRNA NR2F2-AS1 in gastric cancer progression and its association with the clinicopathological characteristics of patients. METHODS: Bioinformatics databases were used to predict the expression levels and interactions between the studied factors to achieve this objective. The expression pattern of NR2F2-AS1/miR- 320b/BMI1 in 40 pairs of tumor and adjacent normal tissues was examined using RT-PCR, IHC, and western blot. The correlation, ROC curve, and survival analyses were also conducted for the aforementioned factors. RESULTS: The results showed an increase of more than 2-fold for BMI-1 and lncRNA NR2F2-AS1 in lower stages, and the elevation continued with the increasing stage of the disease. This correlated with significant downregulation of miR-320b and PTEN, indicating their association with gastric cancer progression and decreased patient survival. LncRNA NR2F2-AS1 acts as an oncogene by influencing the level of miR-320b, altering the amount of BMI1. A reduction in the amount of miR-320b against lncRNA NR2F2-AS1 and BMI1 directly correlates with a reduced overall survival rate of patients, especially if this disproportion is more than 3.0. ROC curve analysis indicated that alteration in the lncRNA NR2F2-AS1 level showed more than 98.0% sensitivity and specificity to differentiate the lower from higher stages of GC and predict the early onset of metastasis. CONCLUSION: In conclusion, these results suggest that NR2F2-AS1/miR-320b/BMI1 has the potential to be a prognostic as well as diagnostic biomarker for gastric cancer.
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Previous studies have supported a tumor-suppressive role of semaphorin 3A (SEMA3A) in several tumors including oral squamous cell carcinoma (OSCC). However, in-depth characterization of the role of SEMA3A in OSCC and the underlying molecular mechanisms is lacking. Gene and protein expressions were detected using quantitative real-time PCR, western blot assay, and immunohistochemistry. OSCC cell metastasis was evaluated using Transwell and angiogenesis of human umbilical vein endothelial cells (HUVECs) was determined using tube formation assay. The interactions among molecules were predicted using bioinformatics analysis and validated using luciferase activity experiment and RNA immunoprecipitation assay. Pulmonary metastasis was evaluated using hematoxylin and eosin staining after constructing a lung metastasis tumor model in mice. SEMA3A expression was decreased in OSCC cells and its overexpression led to suppression of epithelial-mesenchymal transition (EMT), migration, and invasion of OSCC cells and angiogenesis of HUVECs. miR-32-5p was identified as an upstream molecule of SEMA3A and long non-coding RNA NR2F2 antisense RNA 1 (NR2F2-AS1) was validated as an upstream gene of miR-32-5p. Further experiments revealed that the inhibitory effects of NR2F2-AS1 overexpression on EMT, migration, invasion of OSCC cells, and angiogenesis of HUVECs as well as tumor growth and metastasis in mice were mediated via the miR-32-5p/SEMA3A axis. To conclude, NR2F2-AS1 may attenuate OSCC cell metastasis and angiogenesis of HUVECs and suppress tumor growth and metastasis in mice via the miR-32-5p/SEMA3A axis.
Assuntos
Carcinoma de Células Escamosas , Regulação Neoplásica da Expressão Gênica , Células Endoteliais da Veia Umbilical Humana , MicroRNAs , Neoplasias Bucais , RNA Longo não Codificante , Semaforina-3A , Humanos , MicroRNAs/genética , MicroRNAs/metabolismo , Neoplasias Bucais/patologia , Neoplasias Bucais/genética , Neoplasias Bucais/metabolismo , Animais , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo , Semaforina-3A/metabolismo , Semaforina-3A/genética , Carcinoma de Células Escamosas/genética , Carcinoma de Células Escamosas/patologia , Carcinoma de Células Escamosas/metabolismo , Linhagem Celular Tumoral , Camundongos , Células Endoteliais da Veia Umbilical Humana/metabolismo , Progressão da Doença , Transição Epitelial-Mesenquimal/genética , Movimento Celular , Neovascularização Patológica/genética , Neovascularização Patológica/metabolismo , Camundongos NusRESUMO
OBJECTIVE: This study aimed to investigate the role of lncRNA NR2F2-AS1 in oral squamous cell carcinoma cells (OSCC). MATERIALS AND METHODS: The TCGA datasets were used to explore the differential expression of NR2F2-AS1 in OSCC. To further explore the potential interaction between NR2F2-AS1 and miR-494, SCC090 cells were transfected with the NR2F2-AS1 expression vector, NR2F2-AS1 siRNA, and a miR-494 mimic. The effect of NR2F2-AS1 on miR-494 methylation was evaluated by performing methylation-specific PCR (MSP). Cell Counting Kit-8 (CCK-8) assay was used to assess the effects of NR2F2-AS1 silencing and miR-494 and NR2F2-AS1 overexpression on OSCC cell proliferation. RESULTS: NR2F2-AS1 expression was downregulated in OSCC and positively correlated with miR-494 expression. In OSCC cells, NR2F2-AS1 overexpression upregulated miR-494 level, while NR2F2-AS1 silencing decreased miR-494 expression. MSP results showed that NR2F2-AS1 overexpression decreased miR-494 methylation while NR2F2-AS1 silencing increased miR-494 methylation. In addition, NR2F2-AS1 silencing increased OSCC cell proliferation rate while overexpression of miR-494 and NR2F2-AS1 decreased OSCC cell proliferation. Furthermore, miR-494 overexpression attenuated the effects of NR2F2-AS1 silencing on cell proliferation. CONCLUSION: NR2F2-AS1 may inhibit miR-494 methylation to regulate cell proliferation in OSCC. AVAILABILITY OF DATA AND MATERIALS: The analyzed data sets generated during the study are available from the corresponding author upon reasonable request.
Assuntos
Neoplasias de Cabeça e Pescoço , MicroRNAs , Neoplasias Bucais , RNA Longo não Codificante , Fator II de Transcrição COUP/genética , Carcinoma de Células Escamosas , Linhagem Celular Tumoral , Proliferação de Células , Regulação Neoplásica da Expressão Gênica , Humanos , Metilação , MicroRNAs/genética , MicroRNAs/metabolismo , Neoplasias Bucais/genética , RNA Longo não Codificante/metabolismo , Carcinoma de Células Escamosas de Cabeça e PescoçoRESUMO
Long non-coding RNA (LncRNA) is a new type of non-coding RNA whose transcription is more than 200 nucleotides in length and can be up to 100 kb. The crucial regulatory function of lncRNAs in different cellular processes is now notable in many human diseases, especially in different steps of tumorigenesis, making them clinically significant. This research tried to collect all evidence obtained so far regarding Nuclear Receptor subfamily 2 group F member 2 Antisense RNA 1 (NR2F2-AS1) to explore its role in carcinogenesis and molecular mechanism in several cancers. Collecting evidence value an oncogenic role for NR2F2-AS1, whose dysregulation changes the status for cancerous cells to gain the supremacy toward cellular proliferation, dissemination, and ultimately migration. The NR2F2-AS1 acts as competitive endogenous RNA (ceRNA) and contains several microRNA response elements (MREs) for different microRNAs involved in various pathways such as PI3K/AKT, Wnt/ß-catenin, and TGF-ß. This clinically makes NR2F2-AS1 a remarkable lncRNA which contributes to cancer progression and invasion and perhaps could be a candidate as a prognostic marker or even a therapeutic target.
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MicroRNAs , RNA Longo não Codificante , Fator II de Transcrição COUP/genética , Fator II de Transcrição COUP/metabolismo , Carcinogênese/genética , Carcinogênese/patologia , Movimento Celular/genética , Proliferação de Células/genética , Regulação Neoplásica da Expressão Gênica/genética , Humanos , MicroRNAs/genética , MicroRNAs/metabolismo , Fosfatidilinositol 3-Quinases/metabolismo , RNA Antissenso , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismoRESUMO
Non-small cell lung cancer (NSCLC) is one type of the most common cancers, which results in the major death worldwide. This study focuses on the understanding of the molecular mechanism of lncRNA NR2F2-AS1 and its regulation on epithelial-mesenchymal transition (EMT) in the development of NSCLC. Expressions of lncRNA NR2F2-AS1, miR-545-5p, c-Met, biliverdin reductase (BVR), ATF-2 and EMT-related markers in NSCLC tissues and cells were measured by western blotting and RT-qPCR assays. The impact of lncRNA NR2F2-AS1 and miR-545-5p on the cell proliferation, migration, invasion and EMT were analyzed by CCK-8, colony formation, wound healing and transwell assays. The interactions among lncRNA NR2F2-AS1, miR-545-5p and c-Met predicted by bioinformatic analysis were evaluated through dual luciferase reporter assay and fluorescence in situ hybridization (FISH). After generating tumor xenografts, immunohistochemistry was utilized to measure the expression of Ki-67 and EMT-related proteins in vivo. Our results showed that lncRNA NR2F2-AS1, c-Met, BVR and ATF-2 were overexpressed while miR-545-5p was silenced in NSCLC tissues and cells. Silencing of lncRNA NR2F2-AS1 or upregulating miR-545-5p significantly inhibited the cell proliferation, migration, invasion and EMT process. The EMT process could be inhibited by suppressing c-Met/BVR/ATF-2 axis. The tumor xenograft experiments demonstrated that the tumor growth and EMT process were significantly inhibited by silencing lncRNA NR2F2-AS1 or overexpression of miR-545-5p in vivo. LncRNA NR2F2-AS1 promoted the NSCLC development through suppressing miR-545-5p to activate EMT process through c-Met/BVR/ATF-2 axis. Our study indicated that lncRNA NR2F2-AS1 and miR-545-5p could be used as potential therapeutic targets to improve NSCLC treatment.
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Cervical cancer is one of the most frequent malignant tumors in female. Increasing studies have demonstrated that long noncoding RNAs (lncRNAs) play a key role in the development of multiple cancers. Although some studies have confirmed that lncRNA NR2F2 antisense RNA 1 (NR2F2-AS1) is a pro-cancer gene in many cancers, the molecular mechanism of NR2F2-AS1 in cervical cancer has not been completely elucidated. In the present study, our results revealed that NR2F2-AS1 expression was up-regulated in cervical cancer tissues and cells, notably in patients with advanced cervical cancer. NR2F2-AS1 accelerated progression of cervical cancer by facilitating cell proliferation, migration, invasion, and EMT process, but inhibiting cell apoptosis. Moreover, NR2F2-AS1 acted as a molecular sponge of miR-4429 and methyl-CpG-binding domain protein 1 (MBD1) was a downstream target of miR-4429 in cervical cancer. Furthermore, there was a negative correlation between miR-4429 expression and NR2F2-AS1 or MBD1 expression in tumor tissues. Rescue experiments confirmed that MBD1 overexpression partly rescued NR2F2-AS1 knockdown-mediated inhibition of progression in cervical cancer. To sum up, these results suggested the potential mechanism of NR2F2-AS1 in cervical cancer and revealed that NR2F2-AS1 exerted its carcinogenic effect via regulating miR-4429/MBD1 axis, indicating a promising insight into the therapeutic target of cervical cancer.
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Proliferação de Células , Proteínas de Ligação a DNA/metabolismo , MicroRNAs/metabolismo , RNA Longo não Codificante/metabolismo , Fatores de Transcrição/metabolismo , Neoplasias do Colo do Útero/metabolismo , Apoptose , Movimento Celular , Proteínas de Ligação a DNA/genética , Progressão da Doença , Transição Epitelial-Mesenquimal , Feminino , Regulação Neoplásica da Expressão Gênica , Células HeLa , Humanos , MicroRNAs/genética , Invasividade Neoplásica , RNA Longo não Codificante/genética , Transdução de Sinais , Fatores de Transcrição/genética , Neoplasias do Colo do Útero/genética , Neoplasias do Colo do Útero/patologiaRESUMO
Background: Zhang et al. characterized a novel oncogenic long noncoding RNA (lncRNA) named NR2F2-AS1 in lung cancer. In this study, the role of lncRNA NR2F2-AS1 in clear cell renal cell carcinoma (ccRCC) was explored. Materials and Methods: Levels of NR2F2-AS1 and Rac1 mRNA expression in both cancer and noncancer tissues from 60 patients with ccRCC were measured by performing RT-qPCR. NR2F2-AS1 siRNA silencing and overexpression experiments were performed to analyze the role of NR2F2-AS1 in regulating Rac1 expression. Cell stemness was analyzed by stemness assay. Results: NR2F2-AS1 was upregulated in ccRCC, and high NR2F2-AS1 expression levels in ccRCC tissues were associated with poor survival. Rac1 was also upregulated in ccRCC and positively correlated with NR2F2-AS1. In ccRCC cells, NR2F2-AS1 overexpression mediated the upregulation of Rac1, whereas NR2F2-AS1 siRNA was accompanied by Rac1 downregulation. NR2F2-AS1 and Rac1 overexpression resulted in the increased ccRCC cell stemness, whereas NR2F2-AS1 and Rac1 siRNA silencing played an opposite role. Rac1 overexpression inhibited the role of NR2F2-AS1 siRNA silencing. Conclusions: NR2F2-AS1 may upregulate Rac1 to increase cancer stemness in ccRCC.
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Fator II de Transcrição COUP/genética , Carcinoma de Células Renais/genética , Neoplasias Renais/genética , RNA Longo não Codificante/genética , Proteínas rac1 de Ligação ao GTP/genética , Adulto , Carcinoma de Células Renais/patologia , Feminino , Humanos , Neoplasias Renais/patologia , Masculino , Pessoa de Meia-Idade , Regulação para CimaRESUMO
The novel long non-coding RNA NR2F2-AS1 has been characterized as an oncogene in lung cancer. The present study aimed to investigate the role of NR2F2-AS1 in nasopharyngeal carcinoma (NPC). The results demonstrated that expression of NR2F2-AS1 and phosphatase and tensin homolog (PTEN) were negatively associated with each other in NPC tissues. Furthermore, upregulated NR2F2-AS1 expression levels and downregulated PTEN expression levels in NPC tissues predicted less favorable survival outcomes in patients with NPC. Transfection of NPC cells with NR2F2-AS1 small interfering RNA resulted in increased expression of PTEN. In addition, NR2F2-AS1 silencing and PTEN overexpression resulted in decreased proliferation and an increase in the apoptotic rate of NPC cells. In conclusion, NR2F2-AS1 downregulation decreased proliferation and increased apoptosis of NPC cells via upregulation of PTEN.
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PURPOSE: LncRNA NR2F2-AS1 has been characterized as an oncogenic lncRNA in non-small cell lung cancer. This study aims to explore the role of NR2F2-AS1 in colorectal cancer (CRC). METHODS: All CRC patients (n=60, 35 males and 25 females, 40 to 68 years old) in this study were enrolled in Changzhou No.2 People's Hospital of Nanjing Medical University during the time period between July 2011 and December 2013. Tumor samples, CRC cells, vectors, transient transfections, RT-qPCR, western-blotting, as well as measurements of cell cycle, apoptosis and cell proliferation assay were carried out during the research. RESULTS: Our data showed that NR2F2-AS1 was upregulated in CRC and CRC patients with high levels of NR2F2-AS1 showed a low overall survival rate. Cyclin D1 was also upregulated in CRC and a positive correlation was found between Cyclin D1 and NR2F2-AS1. In CRC cells, NR2F2-AS1 siRNA silencing mediated the downregulation of Cyclin D1 and G0/G1 arrest, while Cyclin D1 overexpression rescued G0/G1 arrest caused by NR2F2-AS1 siRNA silencing. CONCLUSION: Our results indicated that NR2F2-AS1 silencing mediates the downregulation of Cyclin D1 to induce G0/G1 arrest in colorectal cancer.
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BACKGROUND/AIM: Hemangiomas are benign neoplastic proliferations of blood vessels. Cytogenetic information on hemangiomas is limited to four tumors with abnormal karyotypes. We report here a solitary chromosomal translocation and its molecular consequence in a hemangioma. MATERIALS AND METHODS: A cavernous hemangioma was extirpated from the foot of a 62 years old man and genetically studied with cytogenetic and molecular genetic methodologies. RESULTS: G-Banding analysis of short-term cultured tumor cells yielded the karyotype 46,Y,t(X;15)(q22;q26)[4]/46,XY[12]. RNA sequencing detected fusion of the collagen type IV alpha 5 chain gene (COL4A5 on Xq22.3) with intronic sequences of nuclear receptor subfamily 2 group F member 2 antisense RNA 1 (NR2F2-AS1 on 15q26.2) resulting in a putative COL4A5 truncated protein. The fusion was verified by RT-PCR together with Sanger sequencing and FISH analyses. CONCLUSION: The involvement of COL4A5 indicates that some hemangiomas have pathogenetic similarities with other benign tumors such as leiomyomas and subungual exostosis.