Tumour-derived exosome SNHG17 induced by oestrogen contributes to ovarian cancer progression via the CCL13-CCR2-M2 macrophage axis.

Oestrogen is known to be strongly associated with ovarian cancer. There was much work to show the importance of lncRNA SNHG17 in ovarian cancer. However, no study has revealed the molecular regulatory mechanism and functional effects between oestrogen and SNHG17 in the development and metastasis of ovarian cancer. In this study, we found that SNHG17 expression was significantly increased in ovarian cancer and positively correlated with oestrogen treatment. Oestrogen could promote M2 macrophage polarization as well as ovarian cancer cells SKOV3 and ES2 cell exosomal SNHG17 expression. When exposure to oestrogen, exosomal SNHG17 promoted ovarian cancer cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) in vitro, and tumour growth and lung metastasis in vivo by accelerating M2-like phenotype of macrophages. Mechanically, exosomal SNHG17 could facilitate the release of CCL13 from M2 macrophage via the PI3K-Akt signalling pathway. Moreover, CCL13-CCR2 axis was identified to be involved in ovarian cancer tumour behaviours driven by oestrogen. There results demonstrate a novel mechanism that exosomal SNHG17 exerts an oncogenic effect on ovarian cancer via the CCL13-CCR2-M2 macrophage axis upon oestrogen treatment, of which SNHG17 may be a potential biomarker and therapeutic target for ovarian cancer responded to oestrogen.

Palbociclib sensitizes ER-positive breast cancer cells to fulvestrant by promoting the ubiquitin-mediated degradation of ER-α via SNHG17/Hippo-YAP axis.

PURPOSE: Endocrine therapy is the anti-tumor therapy for human breast cancer but endocrine resistance was a major burden. It has been reported that Palbociclib and fulvestrant can be used in combination for the treatment of patients who are experiencing endocrine resistance. However, the underlying mechanism is unclear. In this study, we aimed to investigate the mechanism by which Palbocicilib affected ER-positive breast cancer, combined with fulvestrant. METHODS: We first detected the effect of palbociclib on cell survival, growth and cycle distribution separately by MTT, colony formation and flow cytometry. Then SNHG17 was screened as palbociclib-targeted LncRNA by LncRNA-seq, and the SNHG17-targeted mRNAs were selected by mRNA-seq for further determination. Subsequently, the underlying mechanism by which palbociclib promoted the cytotoxicity of fulvestrant was confirmed by qRT-PCR, western blot, and immunoprecipitation. Eventually, the xenograft model and immunohistochemistry experiments were used to validate the sensitization effect of palbociclib on fulvestrant and its mechanism in vivo. RESULTS: Palbociclib significantly enhanced the cytotoxicity of fulvestrant in fulvestrant-resistant breast cancer cell lines. Interestingly, this might be related to the lncRNA SNHG17 and the Hippo signaling pathway. And our subsequent western blotting experiments confirmed that overexpressing SNHG17 induced the down-regulation of LATS1 and up-regulated YAP expression. Furthermore, we found that the increased sensitivity of breast cancer cells was closely associated with the LATS1-mediated degradation of ER-α. The following animal experiments also indicated that overexpressing SNHG17 obviously impaired the anti-cancer effect of co-treatment of palbociclib and fulvestrant accompanied by decreased LATS1 and increased ER-α levels. CONCLUSION: Palbociclib might sensitize the cytotoxicity of fulvestrant in ER-positive breast cancer cells by down-regulating SNHG17 expression, and then resulted in the LATS1-inactivated oncogene YAP and LATS1-mediated degradation of ER-α.

SNHG17 alters anaerobic glycolysis by resetting phosphorylation modification of PGK1 to foster pro-tumor macrophage formation in pancreatic ductal adenocarcinoma.

BACKGROUND: Within the tumor immune microenvironment (TME), tumor-associated macrophages (TAMs) are crucial in modulating polarization states to influence cancer development through metabolic reprogramming. While long non-coding RNAs (lncRNAs) have been shown to play a pivotal role in the progression of various cancers, the underlying mechanisms by which lncRNAs alter M2 polarization through macrophage metabolism remodeling remain unelucidated. METHODS: RNA sequencing was used to screen for differentially expressed lncRNAs in TAMs and normal tissue-resident macrophages (NTRMs) isolated from pancreatic ductal adenocarcinoma (PDAC) tissues, whilst RT-qPCR and FISH were employed to detect the expression level of SNHG17. Moreover, a series of in vivo and in vitro experiments were conducted to assess the functions of SNHG17 from TAMs in the polarization and glycolysis of M2-like macrophages and in the proliferation and metastasis of pancreatic cancer cells (PCs). Furthermore, Western blotting, RNA pull-down, mass spectrometry, RIP, and dual-luciferase assays were utilized to explore the underlying mechanism through which SNHG17 induces pro-tumor macrophage formation. RESULTS: SNHG17 was substantially enriched in TAMs and was positively correlated with a worse prognosis in PDAC. Meanwhile, functional assays determined that SNHG17 promoted the malignant progression of PCs by enhancing M2 macrophage polarization and anaerobic glycolysis. Mechanistically, SNHG17 could sponge miR-628-5p to release PGK1 mRNA and concurrently interact with the PGK1 protein, activating the pro-tumorigenic function of PGK1 by enhancing phosphorylation at the T168A site of PGK1 through ERK1/2 recruitment. Lastly, SNHG17 knockdown could reverse the polarization status of macrophages in PDAC. CONCLUSIONS: The present study illustrated the essential role of SNHG17 and its molecular mechanism in TAMs derived from PDAC, indicating that SNHG17 might be a viable target for PDAC immunotherapy.

Integrated analysis reveals a potential cuproptosis-related ceRNA axis SNHG17/miR-29a-3p/GCSH in prostate adenocarcinoma.

Cuproptosis is a novel form of programmed cell death. The role and mechanism of cuproptosis-related genes in prostate adenocarcinoma have not been fully understood. In this study, a series of bioinformatic analyses were performed. Consequently, glycine cleavage system protein H with high expression and unfavorable prognosis was regarded as the most potential cuproptosis-related gene in prostate adenocarcinoma. Moreover, glycine cleavage system protein H might be a promising indicator for predicting leuprolide sensitivity in prostate adenocarcinoma and three potential drugs targeting glycine cleavage system protein H were identified. Enrichment analysis revealed that glycine cleavage system protein H-correlated genes were significantly enriched in tricarboxylic acid cycle-related pathways. Subsequently, small nucleolar RNA host gene 17/miR-29a-3p axis was found to partially account for overexpression of glycine cleavage system protein H in prostate adenocarcinoma. Collectively, the current study elucidated a potential cuproptosis-related competing endogenous RNA axis small nucleolar RNA host gene 17/miR-29a-3p/glycine cleavage system protein H in prostate adenocarcinoma.

Long non-coding RNA SNHG17 contributes to the progression of pancreatic adenocarcinoma by modulating miR-32-5p/EZH2/STAT3 signaling.

BACKGROUND: Adenocarcinoma of the pancreas (PAAD) is one of the most malignant tumors in the gastrointestinal tract. Long-chain noncoding RNAs (lncRNAs) are non-coding RNAs that are expressed in a variety of cancers. The purpose of this study is to study the expression, biology functions, and molecular mechanism of lncRNA SNHG17 in PAAD. METHODS: In this study, qRT-PCR was used to measure the relative expression of SNHG17 and miR-32-5p in PAAD. In order to investigate the effect of SNHG17 and miR-32-5p on the proliferation, migration and invasion of PAAD cells, we performed a variety of tests including CCK-8, colony formation, scratch and transwell assays. Furthermore, SNHG17 and miR-32-5p interactions were confirmed by a luciferase reporter gene test. RESULTS: Our results indicate that the expression of SNHG17 in PAAD is elevated, and in vitro studies have shown that SNHG17 enhances the proliferation of PAAD cells, Mechanistically, it has been shown that SNHG17 can direct target miR-32-5p in PAAD cells, thus promoting the proliferation of PAAD cells, migration, and invasion. Furthermore, SNHG17 has been found to activate EZH2/STAT3 signaling pathway through miR-32-5p in PAAD cells. CONCLUSION: Our results show that SNHG17 plays a key role in the progression of PAAD by activating STAT3 signaling via regulation of miR-32-5p and EZH2.Identifying these new regulatory pathways may shed light on the underlying mechanism of PAAD and offer a potential therapeutic target for this fatal disease.

Silencing of lncRNA SNHG17 inhibits the tumorigenesis of epithelial ovarian cancer through regulation of miR-485-5p/AKT1 axis.

BACKGROUND: Epithelial ovarian cancer (EOC) stands up for about 90% of ovarian cancer cases, which is the frequent cause of death among women. LncRNAs are involved in progression of EOC. Meanwhile, lncRNA SNHG17 was upregulated in EOC, while the detailed function of SNHG17 in EOC remains unclear. METHODS: Protein and mRNA levels were assessed by western blot and RT-qPCR, respectively. The function of SNHG17 in EOC cells was tested by CCK-8, Ki-67 staining, flow cytometry and transwell assay. Dual luciferase was applied for assessing the relation among SNHG17, miR-485-5p and AKT1. Furthermore, in vivo experiments were applied to test the impact of SNHG17 in EOC. RESULTS: SNHG17 knockdown reduced the proliferation and promoted the apoptosis of EOC cells. Consistently, si-SNHG17 obviously reduced the invasion and epithelial-to-mesenchymal transition (EMT) process of EOC cells. MiR-485-5p was proved to be the target miRNA of SNHG17, and SNHG17 negatively regulated the level of miR-485-5p. MiR-485-5p inhibitor significantly abolished the anti-tumor impact of si-SNHG17 on EOC. AKT1 was identified to be targeted by miR-485-5p, and miR-485-5p negatively modulated AKT1 and p-mTOR levels. Moreover, miR-485-5p mimics reduced the proliferation, migration and promoted the apoptosis of EOC cells via targeting AKT1. Furthermore, si-SNHG17 markedly suppressed EOC growth in vivo. CONCLUSION: SNHG17 silencing inhibits the development of EOC via regulation of miR-485-5p/AKT1 axis. Thus, our study might supply a novel strategy against EOC.

Enabling factor for cancer hallmark acquisition: Small nucleolar RNA host gene 17.

The role of long non-coding RNA (lncRNA) in human tumors has gradually received increasing attention in recent years. Particularly, the different functions of lncRNAs in different subcellular localizations have been widely investigated. The upregulation of lncRNA small nucleolar RNA host gene 17 (SNHG17) has been observed in various human tumors. Growing evidence has proved that SNHG17 plays a tumor-promoting role in tumorigenesis and development. This paper describes the molecular mechanisms by which SNHG17 contributes to tumor formation and development. The different functions of SNHG17 in various subcellular localizations are also emphasized: its function in the cytoplasm as a competing endogenous RNA (ceRNA), its action in the nucleus as a transcriptional coactivator, and its function through the polycomb repressive complex 2 (PRC2)-dependent epigenetic modifications that regulate transcriptional processes. Finally, the correlation between SNHG17 and human tumors is summarized. Its potential as a novel prognostic and diagnostic biomarker for cancer is explored especially.

Low SP1 SUMOylation-dependent SNHG17 upregulation promotes drug resistance of gastric cancer through impairing hsa-miR-23b-3p-induced Notch2 inhibition.

OBJECTIVE: Specificity protein 1 (SP1), a transcription factor mediated by SUMOylation modifiers, is upregulated in gastric cancer (GC) and shares negative correlation with patient prognosis. Here, we paid main attention to the role of SP1 SUMOylation in the drug resistance of GC cells and the possible long non-coding RNA (lncRNA) SNHG17/microRNA-23b-3p (miR-23b-3p)/Notch2 network engaged in this process. METHODS: Tumor tissues and non-tumor tissues were isolated from GC patients who received treatment with capecitabine and cisplatin (DDP). Co-immunoprecipitation was utilized to detect the SUMOylation level of SP1. Using gain- and loss-of-function approaches, we assessed the impacts of SNHG17/miR-23b-3p/Notch2 on sensitivity of DDP-resistant GC cells in vitro and in vivo. A series of assays such as luciferase activity detection and RNA pull-down were conducted for mechanistic exploration. RESULTS: SP1 expression was increased due to low SP1 SUMOylation level in the recurrent GC tissues. This increase led to upregulated SNHG17 expression and SP1 binding sites existed in the SNHG17 promoter. In addition, SNHG17 could bind to miR-23b-3p while miR-23b-3p targeted Notch2. Loss of SNHG17 reduced the resistance of DDP-resistant GC cells to DDP, which was achieved through miR-23b-3p-dependent Notch2 inhibition. Finally, SP1 silencing attenuated the resistance of GC to DDP in mice. CONCLUSION: Low SP1 SUMOylation induces SNHG17 upregulation and blocks miR-23b-3p-induced Notch2 inhibition, contributing to the resistance of GC to DDP. This study may aid in the development of therapeutic targets overcoming the chemoresistance of GC.

COMMD2 Upregulation Mediated by an ncRNA Axis Correlates With an Unfavorable Prognosis and Tumor Immune Infiltration in Liver Hepatocellular Carcinoma.

Liver hepatocellular carcinoma (LIHC) seriously endangers the health and quality of life of individuals worldwide. Increasing evidence has underscored that the copper metabolism MURR1 domain (COMMD) family plays important roles in tumorigenesis. However, the specific role, biological function, mechanism and prognostic value of COMMD2 and its correlation with immune cell infiltration in LIHC remain unknown. In this study, we first determined the expression and prognostic potential of COMMD2 in human tumors using The Cancer Genome Atlas (TCGA) data and identified COMMD2 as a potential oncogene in LIHC. High COMMD2 expression was associated with pathological tumor stage and metastasis. Subsequently, noncoding RNAs (ncRNAs) upregulating COMMD2 expression were identified by performing expression, correlation, and survival analyses in combination. The CRNDE/LINC00511/SNHG17/HCG18-miR-29c-3p axis was identified as the most likely ncRNA-associated pathway upstream of COMMD2 in LIHC. Next, the expression profiles of COMMD2 and ncRNAs were validated in LIHC tissues and adjacent normal tissues. Furthermore, COMMD2 was significantly positively correlated with tumor immune cell infiltration, immune cell biomarkers, and immune checkpoint molecule expression. Importantly, COMMD2 potentially influenced prognosis by regulating immune cell infiltration in LIHC. Finally, COMMD2 was knocked down in LIHC cell lines using siRNAs for functional assays in vitro, resulting in suppressed cell proliferation and migration. In summary, our findings showed that the ncRNA-mediated upregulation of COMMD2 was associated with an unfavorable prognosis correlated with immune cell infiltration in LIHC.

Long noncoding RNA SNHG17: a novel molecule in human cancers.

Many studies in recent years have found that dysregulation of long non-coding RNAs (lncRNAs) can contribute to disease. Small nucleolar RNA host gene 17 (SNHG17) is a novel cancer-related lncRNA of the SNHG family which is highly expressed in various tumors and may exert oncogenic functions. Several studies have demonstrated that SNHG17 is closely related to the proliferation, migration, invasion, apoptosis, and chemical drug resistance of tumor cells, and clinical studies have found an association between high SNHG17 expression and poor prognosis. In this review, we summarize relevant studies investigating SNHG17, focusing on its biological function as well as its potential value for clinical applications.

SNHG17, as an EMT-related lncRNA, promotes the expression of c-Myc by binding to c-Jun in esophageal squamous cell carcinoma.

Dysregulation of long noncoding RNA SNHG17 is associated with the occurrence of several tumors; however, its role in esophageal squamous cell carcinoma (ESCC) remains obscure. The present study demonstrated that SNHG17 was upregulated in ESCC tissues and cell lines, induced by TGF-ß1, and associated with poor survival. It is also involved in the epithelial-to-mesenchymal transition (EMT) process. The mechanism underlying SNHG17-regulated c-Myc was detected by RNA immunoprecipitation, RNA pull-down, chromatin immunoprecipitation, and luciferase reporter assays. SNHG17 was found to directly regulate c-Myc transcription by binding to c-Jun protein and recruiting the complex to specific sequences of the c-Myc promoter region, thereby increasing its expression. Moreover, SNHG17 hyperactivation induced by TGF-ß1 results in PI3K/AKT pathway activation, promoting cells EMT, forming a positive feedback loop. Furthermore, SNHG17 facilitated ESCC tumor growth in vivo. Overall, this study demonstrated that the SNHG17/c-Jun/c-Myc axis aggravates ESCC progression and EMT induction by TGF-ß1 and may serve as a new therapeutic target for ESCC.

Long Non-Coding RNA Small Nucleolar RNA Host Gene 17 Promotes Hepatocellular Carcinoma Progression by Inhibiting p57 Expression.

OBJECTIVE: Long non-coding RNA (lncRNA) small nucleolar RNA host gene 17 (lncRNA SNHG17) is dysregulated in many types of human tumors and acts as a tumor suppressor or promoter according to the tumor type. However, the role of lncRNA SNHG17 in hepatocellular carcinoma (HCC) has been uninvestigated. MATERIALS: Counting on qRT-PCR assay, lncRNA SNHG17 expression in HCC tissues and cell lines (PLC, Hep3B, Huh7 and 7721) was investigated. By utilizing CCK-8 and flow cytometry assays, cell viability and cell cycle were evaluated. qRT-PCR and western blot was implemented to examine p15, p16, p21, p27 and p57 expression levels in HCC cells. RESULTS: We firstly found that expression levels of lncRNA SNHG17 in HCC tissues and cell lines was higher than that in para-carcinoma tissues and QSG-7701 cells (P<0.05). In addition, we observed that patients with tumor size ≥ 5cm, HCC stages III-IV or poor pathological histological types, lncRNA SNHG17 expression were significantly higher than those with tumor size <5 cm, HCC stages I-II or good histopathological types (P<0.05). In vitro studies showcased that low expression of lncRNA SNHG17 restrained HCC cell proliferation and evoked cell cycle arrest. Further, silence of lncRNA SNHG17 up-regulated p57 expression in HCC cells. CONCLUSIONS: Our study shows that lncRNA SNHG17 plays a role as a tumor promoter in HCC, which may provide new clues for the treatment of HCC.

SNHG17 promotes colorectal tumorigenesis and metastasis via regulating Trim23-PES1 axis and miR-339-5p-FOSL2-SNHG17 positive feedback loop.

BACKGROUND: Small nucleolar RNA host gene (SNHG) long noncoding RNAs (lncRNAs) are frequently dysregulated in human cancers and involved in tumorigenesis and progression. SNHG17 has been reported as a candidate oncogene in several cancer types, however, its regulatory role in colorectal cancer (CRC) is unclear. METHODS: SNHG17 expression in multiple CRC cohorts was assessed by RT-qPCR or bioinformatic analyses. Cell viability was evaluated using Cell Counting Kit-8 (CCK-8) and colony formation assays. Cell mobility and invasiveness were assessed by Transwell assays. Tumor xenograft and metastasis models were applied to confirm the effects of SNHG17 on CRC tumorigenesis and metastasis in vivo. Immunohistochemistry staining was used to measure protein expression in cancer tissues. RNA pull-down, RNA immunoprecipitation, chromatin immunoprecipitation, and dual luciferase assays were used to investigate the molecular mechanism of SNHG17 in CRC. RESULTS: Using multiple cohorts, we confirmed that SNHG17 is aberrantly upregulated in CRC and correlated with poor survival. In vitro and in vivo functional assays indicated that SNHG17 facilitates CRC proliferation and metastasis. SNHG17 impedes PES1 degradation by inhibiting Trim23-mediated ubiquitination of PES1. SNHG17 upregulates FOSL2 by sponging miR-339-5p, and FOSL2 transcription activates SNHG17 expression, uncovering a SNHG17-miR-339-5p-FOSL2-SNHG17 positive feedback loop. CONCLUSIONS: We identified SNHG17 as an oncogenic lncRNA in CRC and identified abnormal upregulation of SNHG17 as a prognostic risk factor for CRC. Our mechanistic investigations demonstrated, for the first time, that SNHG17 promotes tumor growth and metastasis through two different regulatory mechanisms, SNHG17-Trim23-PES1 axis and SNHG17-miR-339-5p-FOSL2-SNHG17 positive feedback loop, which may be exploited for CRC therapy.

Carcinoma-associated fibroblasts promote the proliferation and metastasis of osteosarcoma by transferring exosomal LncRNA SNHG17.

Cancer-associated fibroblasts (CAFs) serve as a predominant regulator in the tumor microenvironment. However, the crosstalk between CAFs and OS cells remains mostly unclear. Recent studies explored that long non-coding RNA (LncRNAs) involved in regulating osteosarcoma (OS) formation and development, but their functions in CAFs are unknown. Here, we first investigated the SNHG17 was upregulated in OS tissues and correlated with the poor prognosis through the integrating clinical data. We then evaluated the function of SNHG17 in vitro using the stable SNHG17-depleted OS cells. HOS cells with SNHG17 knocked down were performed to generate the OS xenograft model. Through immunohistochemistry assay and TUNEL apoptosis assay, the role of SNHG17 on OS development was assessed in vivo. We then examined the SNHG17 expression in exosomes derived from CAFs, normal fibroblasts (NFs), and tumor tissues from the OS clinical samples. The interaction among SNHG17, miR-2861, and MMP2 was predicted by bioinformatics analysis and identified by RIP and luciferase assays. The cell proliferation, migration, and apoptosis of SJSA-1 and HOS cells co-cultured with CAFs-derived exosomes were assessed by CCK-8 and colony formation assays. We found that SNHG17 was upregulated in the tumor tissues and presented a pro-tumorigenic effect on OS both in vitro and in vivo. It also was an essential exosomal cargo of CAFs and could affect OS cell proliferation and migration in vitro. CAFs-released exosomal SNHG17 acted as an essential molecular sponge for miR-2861 in OS cells. Moreover, MMP2 was a direct target of miR-2861 and was regulated by SNHG17. Overall, our findings identified that SNHG17 was an essential exosomal cargo of OS-related CAFs that contributes to proliferation and metastasis of OS, supporting the therapeutic potency of targeting the crosstalk between cancer cells and CAFs.

Long non-coding RNA SNHG17 promotes lung adenocarcinoma progression by targeting the microRNA-193a-5p/NETO2 axis.

Long non-coding RNAs (lncRNAs) play vital roles in human cancers. It has been reported that lncRNA SNHG17 expression is dysregulated in different types of cancer and involved in cancer progression. However, the role of SNHG17 in lung adenocarcinoma (LUAD) remains unclear. The present study aimed to investigate the role of SNHG17 in LUAD. Reverse transcription-quantitative (RT-q) PCR analysis was performed to detect SNHG17 expression in LUAD tissues and cells. The effects of SNHG17 on cancer cell migration, invasion, proliferation and epithelial-to-mesenchymal transition (EMT) were assessed via Transwell, MTT and western blot assays, respectively. The interactions between SNHG17 and microRNA (miRNA/miR)-193a-5p, miR-193a-5p and neuropilin and tolloid-like 2 (NETO2) were assessed via the dual-luciferase reporter assay. NETO2 expression and its potential role in LUAD were analyzed via RT-qPCR analysis and the UALCAN database. The results demonstrated that SNHG17 expression was significantly upregulated in LUAD tissues and cells, and high SNHG17 expression was associated with tumor-node-metastasis stage and poor prognosis of patients with LUAD. SNHG17 knockdown inhibited cell migration, invasion, proliferation and the EMT process. In addition, the results revealed that SNHG17 functions as a competing endogenous RNA of miR-193a-5p. The results of the dual-luciferase reporter assay confirmed that miR-193a-5p can directly target SNHG17. NETO2 was also predicted as a target protein of miR-193a-5p, which was confirmed via the dual-luciferase reporter assay. The roles of NETO2 knockdown in cancer cells were rescued following transfection with miR-193a-5p inhibitor or overexpression of SNHG17. Notably, high NETO2 expression was associated with poor prognosis of patients with LUAD. Bioinformatics analysis demonstrated that the promoter methylation level of NETO2 decreased in LUAD. Taken together, the results of the present study suggest that SNHG17 expression is upregulated in LUAD tissues and cells, and SNHG17 exerts tumor promoting effect by targeting the miR-193a-5p/NETO2 axis.

LncRNA SNHG17 promotes tumor progression and predicts poor survival in human renal cell carcinoma via sponging miR-328-3p.

Accumulating data shows that dysregulation of long non-coding RNAs (lncRNAs) are involved in human tumors' occurrence and progression. Small nucleolar RNA host genes (SNHGs) are recently revealed to play a carcinogenic role in various human neoplasms. However, the functions and underlying mechanisms of lncRNA SNHG17 in renal cell carcinoma (RCC) are still elusive. We analyzed the relationship between SNHG17 expression levels and clinicopathologic characteristics and prognosis in patients with RCC according to TCGA RNA-sequencing data and our cohort data. Loss-of-function and gain-of-function experiments were conducted to examine the biological behaviors of SNHG17 on RCC cell proliferation, migration, invasion, apoptosis, and tumor growth in vivo. The interaction between SNHG17, miR-328-3p, and Histone'sH2Avariant (H2AX) was verified by bioinformatics, dual-luciferase reporter gene, and RNA immunoprecipitation (RIP). Highly expressed SNHG17 was evident in RCC tissue samples and cell lines, and SNHG17 overexpression was related to advanced TNM stage and reduced relapse-free and overall survival of patients with RCC. Knockdown of SNHG17 prohibited malignant phenotypes, whereas ectopic SNHG17 expression showed the opposite effects. More importantly, SNHG17 could upregulate the expression of H2AX by acting as a miR-328-3p sponge. In vivo experiments confirmed that SNHG17 promoted the growth of RCC tumors. SNHG17/miR-328-3p/H2AXaxis might be involved in RCC progression, which provided a potential therapeutic target for RCC.

SNHG17 Serves as an Oncogenic lncRNA by Regulating the miR-361-3p/STC2 Axis in Rectal Cancer.

Long noncoding RNA (lncRNA) have been reported to be crucial regulators for carcinogenesis, including rectal cancer. This work aimed to explore the roles and associated mechanisms of small nucleolar RNA host gene 17 (SNHG17) in rectal cancer. A quantitative real-time polymerase chain reaction was performed to measure the expression level of SNHG17 in rectal cancer tissues and cells. Cell counting kit-8 (CCK-8) assay and flow cytometry assay were conducted to measure the biological roles of SNHG17 in rectal cancer. In addition, luciferase activity reporter assay, RNA immunoprecipitation (RIP) assay, and rescue experiments were conducted to explore the mechanisms of SNHG17 in rectal cancer. The upregulation status of SNHG17 was identified in rectal cancer tissues and cells. Functionally, knockdown the expression of SNHG17 inhibits rectal cancer cell proliferation via stimulating cell apoptosis. In vivo assay showed that the knockdown of SNHG17 inhibits tumor growth. Furthermore, we showed that microRNA-361-3p (miR-361-3p) has decreased expression in tumor tissues and cells, and SNHG17 functions as a sponge for miR-361-3p. The upregulation status of stanniocalcin 2 (STC2) was also found in rectal cancer, and the knockdown of STC2 hinders cancer progression. In conclusion, lncRNA SNHG17 functions as an oncogenic lncRNA in rectal cancer by regulating the miR-361-3p/STC2 axis.

LncRNA SNHG17 Contributes to the Progression of Cervical Cancer by Targeting microRNA-375-3p.

PURPOSE: Cervical cancer is a great threat to women's health all over the world. Non-coding RNAs performed a wide range of functions. This study aimed to clarify the clinical significance and biological function of lncRNA SNHG17 and miRNA-375-3p (miR-375-3p) in cervical cancer (CC). PATIENTS AND METHODS: Blood samples from 124 CC patients and 119 healthy volunteers were collected. The relative expression of SNHG17 and miR-375-3p in CC patient serums and cells was evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). The receiver operating curve (ROC) was plotted for diagnostic value estimation. The CCK-8 and transwell assay were conducted to explore the function of SNHG17 on CC cells. A luciferase reporter assay was carried out to confirm the interaction of SNHG17 and miR-375-3p. Rescue experiments were performed to verify the interaction. RESULTS: SNHG17 showed an ascending expression while miR-375-3p descended in the serum of CC patients. For SNHG17 and miR-375-3p, respectively, the AUC was 0.863 and 0.869, the sensitivity was 84.7% and 75.8%, and the specificity was 78.2% and 86.6%. Knockdown of SNHG17 inhibited proliferation, migration, and invasion of CC cells. Serum SNHG17 expression was negatively correlated with miR-375-3p expression, and miR-375-3p was the target miRNA of SNHG17. Rescue experiments verified the knockdown of SNHG17 inhibited cell growth through repressing miR-375-3p expression. CONCLUSION: SNHG17 and miR-375-3p have the potential to be diagnostic markers for CC. Overexpression of SNHG17 in CC promoted the progression of CC partly via targeting miR-375-3p, implying a novel therapeutic target for CC emerging.

Long non-coding RNA SNHG17 enhances the aggressiveness of C4-2 human prostate cancer cells in association with ß-catenin signaling.

Long non-coding (lnc) RNAs have emerged as important regulators of cancer development and progression. Several lncRNAs have been reported to be associated with prostate cancer (PCa); however, the involvement of lncRNA SNHG17 in PCa remains unclear. In the present study, the mRNA expression level of SNHG17 in 58 pairs of PCa tumor samples and adjacent non-tumor tissues, as well as in PCa tumor cell lines was analyzed. The regulatory effect of SNHG17 on the oncogenic phenotypes of the C4-2 tumor cell line was also investigated. The clinicopathological analysis revealed that SNHG17 mRNA expression level was increased in the PCa tumor samples, and its high expression levels were associated with poor patient outcomes, indicating that SNHG17 may act as a biomarker for the prognosis of PCa. SNHG17 mRNA expression level was also increased in different PCa tumor cell lines. Functionally, SNHG17 increased C4-2 tumor cell growth and aggressiveness by stimulating tumor cell proliferation, survival, invasion and resistance to chemotherapy. Furthermore, SNHG17 promoted in vivo tumor growth in a xenograft mouse model. Notably, the SNHG17-induced in vitro and in vivo oncogenic effects were associated with activation of the ß-catenin pathway. The results from the present study revealed that lncRNA SNHG17 could be an important regulator in the oncogenic properties of human PCa and may; therefore, represent a potential PCa therapeutic target.

lncRNA SNHG17 promotes pancreatic carcinoma progression via cross-talking with miR-942.

OBJECTIVE: Long non-coding RNA (lncRNA) SNHG17 has been shown to modulate the biological behavior of multiple cancers (e.g., colorectal and lung cancers). However, its involvement in pancreatic cancer (PC) has not been explored; therefore, in the present study, we sought to examine this involvement. METHODS: First, the mRNA expression levels of various genes were quantified in PC tissues and cell lines using quantitative reverse-transcription PCR (qRT-PCR). The interaction between SNHG17 and miR-942 was explored by bioinformatics prediction as well as a dual luciferase reporter assay. The proliferation and viability of pancreatic carcinoma cells were examined using cell counting kit-8 and MTT assays, respectively. Cellular migratory and invasive properties were evaluated using transwell migration and wound healing assays. Cell death was measured using flow cytometry. Protein expression was quantified by western blotting. RESULTS: SNHG17 expression was markedly higher in human PC specimens and cell lines than in normal healthy tissues and pancreatic epithelial cells. MiR-942 expression displayed the opposite trend. Bioinformatics prediction and a dual luciferase reporter assay confirmed that SNHG17 serves as a sponge for miR-942. Loss-of-function assay revealed that SNHG17 silencing reduced the proliferation and viability of PC cells, impaired their migratory and invasive capacities, and led to their apoptosis. All these changes could be reversed by miR-942 inhibition. Further mechanical studies showed that SNHG17 silencing decreased the expression of several tumor modulators, including XXX, and this decrease was countered by miR-942 inhibition. CONCLUSION: Our study provides experimental evidence for an interaction between SNHG17 and miR-942, which may unveil a new approach for PC pharmacotherapy.