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LncRNA SNHG5 promotes growth and invasion in melanoma by regulating the miR-26a-5p/TRPC3 pathway.
Onco Targets Ther. 2019; 12:169-179.OT

Abstract

Introduction

Melanoma 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.

Methods

Quantitative 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.

Results

The 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.

Conclusion

SNHG5 promoted melanoma development by inhibiting miR-26a-5p and facilitating TRPC3 expression, highlighting the potential of SNHG5 as a novel target therapy for melanoma.

Authors+Show Affiliations

Department of Dermatology, Nanfang Hospital, Southern Medical University, Guangzhou, China, zengkangall25@163.com. Department of Dermatology, Liuzhou Worker's Hospital, Liuzhou, China.Department of Dermatology, Nanfang Hospital, Southern Medical University, Guangzhou, China, zengkangall25@163.com.Department of Hand and Foot Surgery, Liuzhou Worker's Hospital, Liuzhou, China.Department of Clinical Medical Research Center, The 2nd Clinical Medicine College (Shenzhen People's Hospital) of Jinan University, Shenzhen, China.Department of Dermatology, Nanfang Hospital, Southern Medical University, Guangzhou, China, zengkangall25@163.com.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30636880

Citation

Gao, Jun, et al. "LncRNA SNHG5 Promotes Growth and Invasion in Melanoma By Regulating the miR-26a-5p/TRPC3 Pathway." OncoTargets and Therapy, vol. 12, 2019, pp. 169-179.
Gao J, Zeng K, Liu Y, et al. LncRNA SNHG5 promotes growth and invasion in melanoma by regulating the miR-26a-5p/TRPC3 pathway. Onco Targets Ther. 2019;12:169-179.
Gao, J., Zeng, K., Liu, Y., Gao, L., & Liu, L. (2019). LncRNA SNHG5 promotes growth and invasion in melanoma by regulating the miR-26a-5p/TRPC3 pathway. OncoTargets and Therapy, 12, 169-179. https://doi.org/10.2147/OTT.S184078
Gao J, et al. LncRNA SNHG5 Promotes Growth and Invasion in Melanoma By Regulating the miR-26a-5p/TRPC3 Pathway. Onco Targets Ther. 2019;12:169-179. PubMed PMID: 30636880.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - LncRNA SNHG5 promotes growth and invasion in melanoma by regulating the miR-26a-5p/TRPC3 pathway. AU - Gao,Jun, AU - Zeng,Kang, AU - Liu,Yi, AU - Gao,Lin, AU - Liu,Lishi, Y1 - 2018/12/24/ PY - 2019/1/15/entrez PY - 2019/1/15/pubmed PY - 2019/1/15/medline KW - SNHG5 KW - TRPC3 KW - cutaneum carcinoma KW - lncRNA KW - miR-26a-5p SP - 169 EP - 179 JF - OncoTargets and therapy JO - Onco Targets Ther VL - 12 N2 - Introduction: Melanoma 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. Methods: Quantitative 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. Results: The 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. Conclusion: SNHG5 promoted melanoma development by inhibiting miR-26a-5p and facilitating TRPC3 expression, highlighting the potential of SNHG5 as a novel target therapy for melanoma. SN - 1178-6930 UR - https://www.unboundmedicine.com/medline/citation/30636880/LncRNA_SNHG5_promotes_growth_and_invasion_in_melanoma_by_regulating_the_miR_26a_5p/TRPC3_pathway_ L2 - https://dx.doi.org/10.2147/OTT.S184078 DB - PRIME DP - Unbound Medicine ER -
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