Non-coding RNA SNHG1 Research Articles

Long non-coding RNA SNHG15 regulates cardiomyocyte apoptosis after hypoxia/reperfusion injury via modulating miR-188-5p/PTEN axis

Nowadays the most effective way to cure myocardial infarction (MI) is reperfusion, which inevitably leads to cardiomyocyte apoptosis. In this study, we discussed the functions of SNHG15 in regulating cardiomyocyte apoptosis through the modulation of miR-188-5p/PTEN axis. We examined the links between SNHG15 and miR-188-5p/PTEN in mice with MI. Extensive experiments, measurements and comparisons were performed, including RT-PCR, western blotting, luciferase reporter assay, flow cytometry analysis etc. Through a series of comparisons and analysis, we discovered that SNHG15 could interact with the miR-188-5p/PTEN axis and impact the cellular physiology of cardiomyocyte apoptosis. PTEN was upregulated in hypoxia cells, but this effect was attenuated by miR-188-5p. MiR-188-5p could combine with SNHG15 and PTEN, and form a SNHG15-miR-188-5p-PTEN axis, which regulated the apoptosis of MCs. These results suggest that LncRNA SNHG15 regulates cardiomyocyte apoptosis induced by hypoxia or reperfusion injury through modulating of miR-188-5p/PTEN axis.

The long non-coding RNA SNHG1 promotes bladder cancer progression by interacting with miR-143-3p and EZH2.

The long non‐coding RNA (lncRNA) SNHG1 has been shown to be implicated in the progression of multiple human carcinomas. Nevertheless, the biological functions and potential mechanism of SNHG1 in bladder cancer (BC) are uncharacterized. In the present study, SNHG1 was found to be substantially up‐regulated in BC tissues and cells and was intimately correlated with the TNM stage, lymphatic invasion, metastasis and recurrence‐free survival in BC patients. Down‐regulation of SNHG1 dramatically attenuated the proliferation, migration and invasion of BC cells, whereas the ectopic overexpression of SNHG1 had the opposite effects in vitro. The in vivo experimental results also indicated that SNHG1 down‐regulation hampered the tumour growth and metastasis of BC cells. Mechanistic investigations revealed that SNHG1 enhances HK2 expression by serving as an endogenous sponge to regulate miR‐143‐3p in the cytoplasm of BC cells. In the nucleus, SNHG1 could interact with EZH2 and regulate the histone methylation of the CDH1 promoter, altering the biological behaviours of BC cells. Overall, these findings elucidate an oncologic role of SNHG1 in BC and provide a new therapeutic strategy against BC.

SNHG1 represses the anti-cancer roles of baicalein in cervical cancer through regulating miR-3127-5p/FZD4/Wnt/β-catenin signaling.

Baicalein exhibits anti-cancer roles in several cancers. However, the factors influencing the antitumorigenic efficiencies of baicalein in CC remain largely unclear. Here, we provide convincing evidences that lncRNA SNHG1 attenuates the tumor-suppressive roles of baicalein in CC cell viability, apoptosis, migration, and CC tumor growth. This study further demonstrates that the influences of SNHG1 in the antitumorigenic process of baicalein are achieved through modulating the miR-3127-5p/FZD4Wnt/β-catenin axis. SNHG1 attenuates the repressive role of baicalein on Wnt/β-catenin. Therefore, SNHG1 is a novel modulator of the tumor-suppressive roles of baicalein and SNHG1 represents a therapeutic intervention target to reinforce the tumor-suppressive roles of baicalein in CC.

LncRNA SNHG15 predicts poor prognosis in uveal melanoma and its potential pathways.

To evaluate the role of long noncoding RNA (lncRNA) SNHG15 and its potential pathways in uveal melanoma (UM). The SNHG15 mRNA expression level and corresponding clinicopathological characteristics of 80 patients with UM were obtained from the Cancer Genome Atlas (TCGA) database and further analyzed. The SPSS 24.0 statistical software package was used for statistical analyses. To investigate the potential function of SNHG15 in UM, we conducted in-depth research on Gene Set Enrichment Analysis (GSEA). The univariate analysis revealed that the age, tumor diameter, pathological type, extrascleral extension, cancer status, and high expression of SNHG15 were statistical risk factors for death from all causes. The multivariate analysis suggested that the mRNA expression level of SNHG15 was an independent risk factor for death from all causes, as was age and pathological type. Kaplan-Meier survival analysis confirmed that UM patients with high SNHG15 expression might have a poor prognosis. In addition, SNHG15 was significantly differentially expressed in the different groups of tumor pathologic stage, metastasis and living status. Besides, the logistic regression analysis indicated that high SNHG15 expression group in UM was significantly associated with cancer status, pathologic stage, metastasis, and living status. Moreover, the GSEA indicated the potential pathways regulated by SNHG15 in UM. Our research suggests that SNHG15 may play a vital role as a potential marker in UM that predicts poor prognosis. Besides, GSEA indicates the underlying signaling pathways enriched differentially in SNHG15 high expression phenotype.

Clinicopathological significance and prognosis of long noncoding RNA SNHG16 expression in human cancers: a meta-analysis

BackgroundRecent studies have highlighted the important role of long non-coding RNA SNHG16 in various human cancers. Here, we conducted a meta-analysis to investigate the effect of SNHG16 expression on clinicopathological features and prognosis in patients with different kinds of human cancers.MethodsWe performed a systematic search in electronic databases including PubMed, EMBASE, Cochrane Library and Web of Science, to investigate the potential association between SNHG16 expression and prognostic significance and clinical features in cancer patients. Odds ratios (ORs) or hazards ratios (HRs) with corresponding 95% confidence intervals (95% CIs) were pooled to estimate the prognosis value of SNHG16 by StataSE 15.0 software.ResultsA total of 16 eligible studies with 1299 patients were enrolled in our meta-analysis. The results revealed that increased expression level of SNHG16 was significantly associated with larger tumor size (OR: 3.357; 95% CI: 2.173–5.185; P < 0.001), advanced TNM stage (OR: 2.930; 95% CI: 1.522–5.640; P = 0.001) and poor histological grade (OR: 3.943; 95% CI: 1.955–7.952; P < 0.001), but not correlated with smoking status (P = 0.489), sex (P = 0.932), distant metastasis (P = 0.052), or lymph node metastasis (P = 0.155). Moreover, the pooled HR showed that elevated expression SNHG16 was associated with a significantly poorer overall survival (OS) (HR = 1.866, 95% CI: 1.571–2.216, P < 0.001). For the set of cancer types, high expression of SNHG16 was significantly associated with shorter OS in patients with cancers of the urinary system (HR: 2.523, 95% CI:1.540–4.133; P <0.001), digestive system (HR: 2.406, 95% CI:1.556–3.721; P <0.001), and other cancers (including glioma and non-small cell lung cancer) (HR: 1.786, 95% CI:1.406–2.267; P <0.001).ConclusionsLncRNA SNHG16 overexpression might serve as an unfavorable prognostic factor, which provides a basis for medical workers to evaluate the prognosis of patients and to help the decision-making process.

Long noncoding RNA SNHG12 promotes tumour progression and sunitinib resistance by upregulating CDCA3 in renal cell carcinoma

Renal cell carcinoma (RCC) is one of the most frequently observed malignant tumours in the urinary system and targeted drug resistance is quite common in RCC. Long noncoding RNA SNHG12 (lncRNA SNHG12) has emerged as a key molecule in numerous human cancers, but its functions in renal cell carcinoma (RCC) sunitinib resistance remain unclear. In this study, we found SNHG12 was highly expressed in RCC tissues and in sunitinib-resistant RCC cells and was associated with a poor clinical prognosis. SNHG12 promoted RCC proliferation, migration, invasion and sunitinib resistance via CDCA3 in vitro. Mechanically, SNHG12 bound to SP1 and prevented the ubiquitylation-dependent proteolysis of SP1. Stabilised SP1 bound to a specific region in the promoter of CDCA3 and increased CDCA3 expression. Furthermore, in vivo experiments showed that SNHG12 increased tumour growth and that knocking down SNHG12 could reverse RCC sunitinib resistance. Our study revealed that the lncRNA SNHG12/SP1/CDCA3 axis promoted RCC progression and sunitinib resistance, which could provide a new therapeutic target for sunitinib-resistant RCC.

Long noncoding RNA SNHG14 promotes ovarian cancer cell proliferation and metastasis via sponging miR-219a-5p.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Long noncoding RNA SNHG14 promotes ovarian cancer cell proliferation and metastasis via sponging miR-219a-5p, by L. Li, R. Zhang, S.-J. Li, published in Eur Rev Med Pharmacol Sci 2019; 23 (10): 4136-4142-DOI: 10.26355/eurrev_201905_17915-PMID: 31173283" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/17915.

Long noncoding RNA SNHG14 promotes breast cancer cell proliferation and invasion via sponging miR-193a-3p.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Long noncoding RNA SNHG14 promotes breast cancer cell proliferation and invasion via sponging miR-193a-3p, by S.-D. Xie, C. Qin, L.-D. Jin, Q.-C. Wang, J. Shen, J.-C. Zhou, Y.-X. Chen, A.-H. Huang, W.-H. Zhao, L.-B. Wang, published in Eur Rev Med Pharmacol Sci 2019; 23 (6): 2461-2468. DOI: 10.26355/eurrev_201903_17393. PMID: 30964172" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/17393.

Long Noncoding RNA SNHG15 Serves as an Oncogene and Predicts Poor Prognosis in Epithelial Ovarian Cancer [Expression of Concern

Long Noncoding RNA SNHG15 Serves as an Oncogene and Predicts Poor Prognosis in Epithelial Ovarian Cancer [Expression of Concern

Long non-coding RNA SNHG7 promotes migration and invasion of melanoma via upregulating SOX4.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Long non-coding RNA SNHG7 promotes migration and invasion of melanoma via upregulating SOX4, by C. Zhang, B. Zhu, X.-B. Li, Y.-Q. Cao, J.-C. Yang, X. Li, Y.-X. Liu, Y.-B. Wang, published in Eur Rev Med Pharmacol Sci 2019; 23 (11): 4828-4834-DOI: 10.26355/eurrev_201906_18069-PMID: 31210315" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/18069.

Long noncoding RNA SNHG16 acts as an oncogene in Wilms' tumor through sponging miR-200a-3p.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Long noncoding RNA SNHG16 acts as an oncogene in Wilms' tumor through sponging miR-200a-3p, by X.-S. Zhao, N. Tao, C. Zhang, C.-M. Gong, C.-Y. Dong, published in Eur Rev Med Pharmacol Sci 2020; 24 (8): 4145-4151-DOI: 10.26355/eurrev_202004_20994-PMID: 32373950" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/20994.

Lin28A promotes IRF6-regulated aerobic glycolysis in glioma cells by stabilizing SNHG14

Warburg effect is a hallmark of cancer cells, wherein glycolysis is preferred over oxidative phosphorylation even in aerobic conditions. Reprogramming of glycometabolism is especially crucial for malignancy in glioma. RNA-binding proteins and long noncoding RNAs are important for aerobic glycolysis during malignant transformation. Thus, we determined the expression and function of RNA-binding protein Lin28A, long noncoding RNA SNHG14, and transcription factor IRF6 in human glioma cells to elucidate the mechanism(s) underlying their role in glycolysis. Quantitative real-time polymerase chain reaction and western blotting showed that Lin28A and SNHG14 were overexpressed and IRF6 was downregulated in glioma. Depleting Lin28A from cells decreased the stability and expression of SNHG14. Furthermore, depleting SNHG14 reduced IRF6 mRNA degradation by targeting its 3′ untranslated region and inhibiting STAU1-mediated degradation, thereby increasing the expression of IRF6. PKM2 is an important enzyme in aerobic glycolysis, and GLUT1 is the primary transporter that facilitates glucose uptake. IRF6 inhibited the transcription of PKM2 and GLUT1, thereby impairing glycolysis and cell proliferation and inducing apoptosis in glioma. Notably, depleting Lin28A and SNHG14 and overexpressing IRF6 reduced the growth of xenograft tumors in vivo and prolonged the survival of nude mice. Taken together, our data revealed that the Lin28A/SNHG14/IRF6 axis is crucial for reprogramming glucose metabolism and stimulating tumorigenesis in glioma cells. Thus, targeting this axis might help in the development of a novel therapeutic strategy for glioma metabolism.

Overexpression of long non-coding RNA SNHG16 against cerebral ischemia-reperfusion injury through miR-106b-5p/LIMK1 axis

Long non-coding RNA (LncRNA) involved in types of physiological insults and diseases via regulating the responses of complex molecular, including cerebral ischemia-reperfusion (I/R) injury. LncRNA SNHG16 played a potential role in ketamine-induced neurotoxicity. In this study, we utilized an in vitro cell model of I/R to examine the specific function and mechanism of LncRNA SNHG16 in oxygen-glucose deprivation and reperfusion (OGD/R) induced SH-SY5Y cells. After in vitro treatment of OGD/R, the lower the SH-SY5Y cell survival, the higher cell the apoptosis and increased caspase-3 activity was observed. Also, OGD/R induced endoplasmic reticulum stress (ERS) through increasing GRP78 and CHOP expressions and down-regulated LncRNA SNHG16 in SH-SY5Y cells. Conversely, LncRNA SNHG16 overexpression promoted OGD/R induced SH-SY5Y cell survival, suppressed its apoptosis, and caspase-3 activity. GRP78 and CHOP expressions were significantly suppressed in LncRNA SNHG16 overexpressing cells. MiR-106b-5p expression was increased and LIMK1 expression was down-regulated in OGD/R induced SH-SY5Y cells, and these effects were reversed by LncRNA SNHG16 overexpression, respectively. Moreover, LIMK1 is a direct target of MiR-106b-5p, and knockdown of LIMK1 reversed the effects of LncRNA SNHG16 on OGD/R-induced SH-SY5Y cells biology. Altogether, these results confirmed an important neuroprotection role of LncRNA SNHG16 in OGD/R induced SH-SY5Y cells injury, and miR-106b-5p/LIMK1 signal axis was involved in the action of LncRNA SNHG16.

Up‐regulation of SNHG16 induced by CTCF accelerates cardiac hypertrophy by targeting miR‐182‐5p/IGF1 axis

Long non-coding RNA (lncRNA) SNHG16 has been reported to be significant regulators in multiple cancers. However, never has the relationship between it and cardiac hypertrophy been studied until now. In this study, angiotensin II (Ang II)-treated cardiomyocytes isolated from neonatal mice were used as a model of cardiac hypertrophy in vitro. Real-time quantitative polymerase chain reaction was performed to measure the expression of SNHG16, miR-182-5p, and insulin-like growth factor 1 (IGF1). The relationship between SNHG16 and its downstream genes were corroborated by RNA pull-down and luciferase reporter experiments. Western blot was conducted to detect the expression of markers of hypertrophy. The results disclosed that SNHG16 expression was in a high level in the cardiac hypertrophic model. Down-regulation of SNHG16 could decline the expression of hypertrophic markers and reduce cell surface area induced by Ang II. Moreover, SNHG16 was discovered to be activated by transcription factor CCCTC-binding factor. In addition, SNHG16 could enlarge cell surface area and increase the expression of hypertrophic markers by inhibiting miR-182-5p expression in Ang II-treated cardiomyocytes. Finally, overexpression of IGF1 could rescue the effects of silenced SNHG16 on cardiac hypertrophy cells. In brief, our study illustrated that silenced SNHG16 repressed Ang II-imposed cardiac hypertrophy via targeting miR-182-5p/IGF1 axis.

Long noncoding RNA SNHG14 promotes malignancy of prostate cancer by regulating with miR-5590-3p/YY1 axis.

Studies have demonstrated that long non-coding RNAs (lncRNAs) are important in the development and prognosis of prostate cancer. The aim of this study was to investigate the functions and mechanism of lnc-SNHG14 in prostate cancer. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) or Western blot (WB) were performed to detect mRNA expressions of SNHG14 and miR-5590-3p, and the protein levels of Yin Yang-1 (YY1) in prostate cancer tissues, adjacent tissues, and cancer cell lines. The correlation analysis was used to analyze the correlations between SNHG14, miR-5590-3p, and YY1. Kaplan-Meier survival analysis was used to analyze the overall survival for prostate cancer patients. Cell Counting Kit-8 (CCK-8) assay was performed to measure cell proliferation ability and flow cytometry assay was used to detect cell apoptotic rate. Besides, transwell assay was used to measure cell invasion ability. In addition, WB was performed to measure protein expressions in prostate cancer cell lines. Finally, Luciferase reporter assay was performed to verify the binding sites between SNHG14 and miR-5590-3p, miR-5590-3p, and YY1. The results showed that SNHG14 was significantly increased in prostate cancer tissues and prostate cancer cell lines, which were related with advanced stage and poor diagnosis for prostate cancer patients. MiR-5590-3p was reduced in prostate cancer tissues and cell lines, which were negatively correlated with SNHG14. YY1 was found to be increased in prostate cancer tissues, which was negatively correlated with miR-5590-3p and positively correlated with SNHG14. Furthermore, SNHG14 knockdown inhibited cell proliferation, invasion, and promoted cell apoptosis in DU145 cells. In addition, protein expressions of Cyclin D1, Bcl-2, and N-cadherin were repressed, and the levels of Bax, Cleaved Caspase-3, and E-cadherin were increased. Besides, miR-5590-3p inhibition promoted cell proliferation and invasion, and inhibited apoptosis in DU145 cells. Importantly, Luciferase reporter assay proved that SNHG14 could directly sponge with miR-5590-3p, which could bind with YY1 and regulate the functions of cancer cell. Finally, we proved that SNHG14 regulated cell proliferation, cell apoptosis, and invasion via miR-5590-3p/ YY1 axis in prostate cancer. Above all, we found that SNHG14 was increased in prostate cancer patients, which was related with future diagnosis for prostate cancer patients. Of note, we discovered that SNHG14 could promote cell proliferation, invasion, and repress cell apoptosis via miR-5590-3p/YY1 axis in prostate cancer, which might provide a new target for treating prostate cancer.

Long Non-Coding RNA SNHG14 Contributes to the Development of Hepatocellular Carcinoma via Sponging miR-217.

BackgroundThousands of long non-coding RNAs (lncRNAs) have been functionally verified as crucial regulators of physiological processes and disease progressions, yet their roles in hepatocellular carcinoma (HCC) have not been clearly illuminated.MethodsWe analyzed the expression of lncRNA-SNHG14 in TCGA data via bioinformatic analysis and detected its expression in HCC specimens by reverse transcription‐quantitative polymerase chain reaction (RT‐qPCR). Loss-of-function experiments were used to study the biological function of SNHG14 in HCC cells. RT-qPCR, Western blotting and dual-luciferase reporter assay were carried out to investigate the molecular mechanism of SNHG14 in HCC.ResultsThe upregulation of lncRNA-SNHG14 was observed in HCC tissues compared with normal tissues via RT-qPCR and bioinformatic analysis of TCGA data. Silencing of SNHG14 inhibited cell proliferation and induced cell apoptosis in HCC cells. microRNA-217 (miR-217), the tumor-suppressive miRNA in HCC, was predicted and confirmed as a miRNA sponged by SNHG14 in HCC cells. Via downregulation of miR-217, SNHG14 increased the expression of several miR-217-related oncogenes and subsequently activated oncogene-related signaling pathways in HCC cells. In addition, inhibition of miR-217 reversed SNHG14 silencing induced decrease of cell proliferation and increase of cell apoptosis. Their association was verified in the published microarray dataset and the collected HCC samples.ConclusionIn summary, SNHG14 is involved in the development of HCC via sponging miR-217 and it may be a biomarker for patients with HCC.

Long non-coding RNA SNHG15 is a competing endogenous RNA of miR-141-3p that prevents osteoarthritis progression by upregulating BCL2L13 expression

Increasing evidence has demonstrated that the dysregulated expression of long noncoding RNAs (lncRNAs) has important roles in the progression of osteoarthritis (OA), but the function of the lncRNA SNHG15 remains unclear. In the present study, we observed that SNHG15 was downregulated in OA cartilage tissues and IL-1β-induced chondrocytes. The lower expression of SNHG15 was negatively associated with the observed modified Mankin scale scores, extracellular matrix (ECM) degradation and chondrocyte apoptosis. Downregulated expression of SNHG15 increased chondrocyte viability and decreased chondrocyte apoptosis and ECM degradation in vitro and reduced damage to articular cartilage in vivo. Mechanistically, we demonstrated that SNHG15 overexpression promotes the expression of BCL2L13 by sponging miR-141-3p. The higher expression of miR-141-3p was negatively correlated with SNHG15 and BCL2L13 levels in OA cartilage tissues, and a positive correlation was also shown between SNHG15 and BCL2L13 levels. Furthermore, ectopic expression of miR-141-3p or knockdown of BCL2L13 expression could both reduce the effects of SNHG15 on chondrocyte proliferation, apoptosis and ECM degradation. Collectively, these findings reveal that SNHG15 inhibits OA progression by acting as an miR-141-3p sponge to promote BCL2L13 expression, suggesting that knockdown of SNHG15 expression in chondrocytes can be a potential therapeutic strategy to ameliorate OA progression.

Long noncoding RNA SNHG16 acts as an oncogene in Wilms' tumor through sponging miR-200a-3p.

Recently, the role of long noncoding RNA (lncRNAs) in tumor progression has attracted much attention. The aim of this study was to investigate the role of lncRNA SNHG16 in the development of Wilms' tumor, and to explore the underlying mechanism. Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was used to detect SNHG16 expression in Wilms' tumor patients' tissues. Function assays, including wound healing assay, and transwell assay, were conducted to detect the changes of biological behaviors in Wilms' tumor cells due to gain or loss of SNHG16. Besides, the luciferase reporter gene assay was performed to explore the underlying mechanism. The expression level of SNHG16 was significantly up-regulated in Wilms' tumor tissues when compared with adjacent tissues. Cell migration and invasion abilities were significantly repressed via down-regulation of SNHG16. However, opposite results were obtained after up-regulation of SNHG16 in vitro. After the down-regulation of SNHG16, the expression of miR-200a-3p increased significantly. However, the expression of miR-200a-3p was remarkably reduced via up-regulation of SNHG16 in vitro. Furthermore, SNHG16 acted as a competing endogenous RNA via sponging miR-200a-3p in Wilms' tumor. SNHG16 induced the metastasis of Wilms' tumor via sponging miR-200a-3p. Our findings might provide a new prospect for the diagnosis and therapy of Wilms' tumor.

High expression of lncRNA-SNHG7 is associated with poor prognosis in hepatocellular carcinoma.

Expression of long non-coding RNA SNHG7 (lncRNA-SNHG7) and its clinical significance in hepatocellular carcinoma (HCC) were explored. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression level of lncRNA-SNHG7 in cancer tissues. Kaplan-Meier curves and multivariate Cox proportional models were used to study the impact on clinical outcome. Expression of lncRNA-SNHG7 was much higher in cancer tissues than that in para-cancer tissues. The lncRNA-SNHG7 expression was correlated with tumor number, lymph node metastasis and clinical stage (P<0.05). In addition, HCC patients with higher lncRNA-SNHG7 expression had significantly poorer progression-free survival time and overall survival time (P<0.001). Both univariate analysis and multivariate analysis indicated that high expression of lncRNA-SNHG7 was an independent predictor of poor prognosis in HCC. LncRNA-SNHG7 might contribute to the development of HCC and serve as a clinical biomarker and a therapeutic target for HCC patients.

Long Noncoding RNA SNHG6 Promotes Carcinogenesis by Enhancing YBX1-Mediated Translation of HIF1α in Clear Cell Renal Cell Carcinoma

Background: Dysregulated expression of long noncoding RNA SNHG6 plays important roles in the oncogenesis of many human cancers while the function of SNHG6 remains unclear in clear cell renal cell carcinoma (ccRCC). In this study, we aimed to assess the role of SNHG6 in the progression of ccRCC. Methods: RNA-Seq data from The Cancer Genome Atlas (TCGA) were analyzed by bioinformatic methods to identify lncRNA dysregulated in ccRCC. The CCK-8, colony formation, Transwell and wound-healing assays were used to assess the biological function of SNHG6 in vitro, and an in vivo xenograft model in nude mice was established. Quantitative real-time PCR and immunohistochemistry (IHC) were used to analyze the expression of SNHG6 in ccRCC tissues. The underlying mechanisms of SNHG6 were investigated using mRNA microarray analyses, Western blotting, RNA pull-down, and RNA immunoprecipitation. Findings: SNHG6 expression was significantly upregulated in ccRCC tissues compared with paired normal renal tissues. High SNHG6 expression was correlated with advanced T stage and poor survival. Further functional experiments demonstrated that knockdown of SNHG6 in ccRCC cells inhibited cell proliferation, migration and invasion in vitro as well as tumor growth and migration in vivo. Mechanistically, SNHG6 bound to YBX1 to act as a complex, thereby enhancing HIF1α translation. Interpretation: SNHG6 promotes ccRCC progression by binding YBX1 and may serve as a novel molecular target for ccRCC therapy. Funding Statement: This work was supported in part by grants from the National Natural Science Foundation of China (No.81903050) and the Science and Technology Commission of Shanghai Municipality (17ZR1417500). Declaration of Interests: The authors declare that they have no conflict of interest. Ethics Approval Statement: The study was approved by the Human Ethics Committee of the Fudan University Shanghai Cancer Center.