SNHG5 promotes proliferation and induces apoptosis in melanoma by sponging miR-155

Liu, Yan; Wang, Suihai; Li, Yue; Tognetti, Linda; Tan, Rui; Zeng, Kang; Pianigiani, Elisa; Mi, Xiangbin; Li, Hui; Fimiani, Michele; Rubegni, Pietro

doi:10.1039/c7ra12520h

Cited by 9 publications

(9 citation statements)

References 31 publications

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“…Additionally, SNHG5 expression was upregulated in bladder cancer, and SNHG5 knockdown repressed cell growth and induced apoptosis in a p27-dependent manner 14. In the current study, SNHG5 expression was found to be upregulated in melanoma tumor tissues and cell lines, and correlated with advanced pathological stages, consistent with a previous study 16…”

Section: Discussionsupporting

confidence: 91%

“…These data uncovered that SNHG5 exerted functions as an oncogene in melanoma by sponging miR-26a-5p. Coincident with our results, Yan et al validated that SNHG5 knockdown suppressed proliferation and facilitated apoptosis in melanoma cells by serving as a molecular sponge of miR-155 16…”

Section: Discussionsupporting

confidence: 90%

“…Ichigozaki et al disclosed that the serum level of SNHG5 was increased in malignant melanoma patients compared with that in normal subjects 15. Also, a recent document revealed that SNHG5 expression was upregulated in melanoma tissues and cells, and SNHG5 knockdown blocked proliferation and induced apoptosis by modulating miR-155 16. Nevertheless, the roles and molecular bases of SNHG5 in melanoma pathogenesis deserve to be further explored.…”

Section: Introductionmentioning

confidence: 99%

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LncRNA SNHG5 promotes growth and invasion in melanoma by regulating the miR-26a-5p/TRPC3 pathway

Gao

Zeng

Liu

et al. 2018

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IntroductionMelanoma has been reported as the most common malignancy in skin cancer. The small nucleolar RNA host gene 5 (SNHG5), an lncRNA, has been proven as a vital regulator in several types of carcinoma. This study was designed to investigate the detailed roles and possible mechanisms of SNHG5 in melanoma progression.MethodsQuantitative real-time PCR (qRT-PCR) analysis was conducted to detect the expression levels of SNHG5, miR-26a-5p and transient receptor potential, canonical 3 (TRPC3) mRNA in melanoma tissues and cells. CCK-8 assay was used to measure the cell viability. Flow cytometry assays were performed to determine the cell cycle distribution and apoptosis. The invasive ability was assessed by a 24-well Transwell insert. Western blot analysis was employed to evaluate the protein expression of TRPC3. Dual luciferase reporter assay, RNA immunoprecipitation (RIP) assay, and RNA pull-down assay were applied to identify the interactions among SNHG5, miR-26a-5p and TRPC3.ResultsThe results showed that SNHG5 expression was increased in melanoma tumor tissues and cell lines. Higher SNHG5 expression was correlated with advanced pathogenic status. Moreover, SNHG5 could serve as a molecular sponge of miR-26a-5p. SNHG5 downregulation repressed proliferation, promoted apoptosis, and decreased invasion in melanoma cells, while these effects were greatly counteracted by miR-26a-5p inhibitor. Furthermore, miR-26a-5p directly targeted TRPC3 to suppress its expression, and this effect was aggravated following SNHG5 downregulation. Also, TRPC3 depletion exerted similar tumor-suppressive functions as SNHG5 knockdown.ConclusionSNHG5 promoted melanoma development by inhibiting miR-26a-5p and facilitating TRPC3 expression, highlighting the potential of SNHG5 as a novel target therapy for melanoma.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

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LncRNA SNHG5 promotes growth and invasion in melanoma by regulating the miR-26a-5p/TRPC3 pathway

Gao

Zeng

Liu

et al. 2018

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“…to exert oncogenic roles in colorectal cancer, melanoma, bladder cancer, and hepatocellular carcinoma (Damas et al, 2016;Ma, Xue, Zeng, & Qiu, 2018;Yan et al, 2018) while inhibits gastric cancer evolution (Zhao et al, 2016). Besides, we reported associations between expression levels of this lncRNA and histological grade, which is in line with findings in hepatocellular carcinoma (Y.…”

Section: Discussionsupporting

confidence: 84%

Assessment of the expression pattern of mTOR‐associated lncRNAs and their genomic variants in the patients with breast cancer

Taherian‐Esfahani

Taheri

Dashti

et al. 2019

Journal Cellular Physiology

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The mechanistic target of rapamycin (mTOR) is a fundamental component of a signaling pathway that is involved in the pathogenesis of breast cancer via different mechanisms. This pathway is functionally linked with a number of small nucleolar RNA host genes (SNHGs). In the present project, we have searched for the expression quantitative trait loci (eQTLs) within SNHGs that are possibly involved in the pathogenesis of breast cancer. Following this in silico step, we have assessed expression levels of mTOR and four SNHGs in malignant and nonmalignant samples obtained from 80 patients with breast cancer. We also genotyped rs4615861 of SNHG3 and rs3087978 of SNHG5 in the peripheral blood of patients. SNHG12 expression was not detected in any of the assessed malignant or nonmalignant tissues. So this gene was excluded from further steps. Expression of mTOR and other three long noncoding RNAs (lncRNAs) were significantly increased in the malignant tissues compared with the nonmalignant tissues. When classifying patients into down-/upregulation categorized based on the transcript levels of each gene in malignant tissue versus nonmalignant tissues, we noticed associations between expression of SNHG1 and stage (p = 0.03), expression of SNHG5 and grade (p = 0.05), as well as between expression of SNHG3 and history of oral contraceptive use (p = 0.04). We also detected higher levels of SNHG3 expression in estrogen receptor/ progesterone receptor (ER/PR) negative tumors compared with the ER/PR positive tumors (p = 0.003 and p = 0.01, respectively). Moreover, there was a trend toward higher expression of this lncRNA in HER2-positive tumors compared with the HER2negative ones (p = 0.07). Combination of transcript levels of all genes could differentiate malignant tissues from nonmalignant tissues with the diagnostic power of 69% (p = 0.0001). The rs3087978 was associated with the expression of mTOR in malignant tissues in a way that TT and TG genotypes were associated with the higher and lower levels of expressions, respectively (p = 0.01). The current study underscores the significance of SNHGs in the pathogenesis of breast cancer. K E Y W O R D Sbreast cancer, lncRNA, mTOR

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“…Additionally, there existed a sponged regulation between lncRNA XIST and miR-155 within breast cancer cells, 13 which provoked a speculation that lncRNA XIST might be implicated in AS aetiology via its sponging miR-155. Concerning another lncRNA studied here, the lncRNA SNHG5 was also suggested to negatively regulate miR-155 expression within melanoma cells, 14…”

Section: Introductionmentioning

confidence: 84%

Dual impacts of lncRNA XIST and lncRNA SNHG5 on inflammatory reaction and apoptosis of endothelial cells via regulating miR‐155/CARHSP1 axis

Song

Yang

Chang

et al. 2020

J Cellular Molecular Medi

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Considering the significance of lncRNA/miRNA axis in explaining atherosclerosis (AS) progression, this investigation was intended to clarify whether lncRNAs XIST/SNHG5 would regulate AS aetiology by sponging miR‐155, an AS‐promoting molecule. We altogether recruited 367 patients who were examined by coronary angiography, and meanwhile, human coronary artery endothelial cells (HCAECs) were purchased to establish cells models via ox‐LDL treatment. The study results indicated that lowly expressed XIST/SNHG5 and highly expressed miR‐155 were frequently detectable among AS patients who showed severe stenosis and possessed high triglyceride (TG), low‐density lipoprotein cholesterol (LDL‐C) and high‐sensitivity C‐reactive protein (hs‐CRP) levels. Besides, HCAECs treated by ox‐LDL released large amounts of inflammatory cytokines, and their apoptosis rate was also raised. Moreover, expressions of XIST and SNHG5 declined markedly within ox‐LDL‐treated HCAECs, whereas miR‐155 expression significantly ascended. Transfection of pcDNA‐XIST and pcDNA‐SNHG5 both reduced the expression of TNF‐α, IL‐6, IL‐8 and IL‐1β within HCAECs and also dampened the apoptotic tendency of HCAECs. Co‐treatment of pcDNA‐XIST and pcDNA‐SNHG5 produced a larger effect on HCAEC activity than pcDNA‐XIST or pcDNA‐SNHG5 alone. Furthermore, miR‐155, modified by XIST and SNHG5, was capable of reversing the impacts of XIST and SNHG5 on HCAEC activity. Eventually, CARHSP1 was activated by XIST and SNHG5, and its overexpression dwindled impacts of miR‐155 mimic on proliferation and inflammation response of HCAECs. In conclusion, targeting XIST and SNHG5 might be an ideal alternative in delaying AS progression, allowing for their repression of downstream miR‐155.

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SNHG5 promotes proliferation and induces apoptosis in melanoma by sponging miR-155

Abstract: Melanoma is the most common malignancy of skin cancer. Small nucleolar RNA host gene 5 (SNHG5), a long non-coding RNA (lncRNA), has been demonstrated to be upregulated in tumor tissues and cells of melanoma.

Cited by 9 publications

References 31 publications

LncRNA SNHG5 promotes growth and invasion in melanoma by regulating the miR-26a-5p/TRPC3 pathway

LncRNA SNHG5 promotes growth and invasion in melanoma by regulating the miR-26a-5p/TRPC3 pathway

Assessment of the expression pattern of mTOR‐associated lncRNAs and their genomic variants in the patients with breast cancer

Dual impacts of lncRNA XIST and lncRNA SNHG5 on inflammatory reaction and apoptosis of endothelial cells via regulating miR‐155/CARHSP1 axis

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