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Updated: Jan 30, 2026
A Robust Discovery Platform for the Identification of Novel Mediators of Melanoma Metastasis
Published on: March 8, 2022
LncRNA SNHG5 promotes growth and invasion in melanoma by regulating the miR-26a-5p/TRPC3 pathway
Jun Gao1,2, Kang Zeng1, Yi Liu3
1Department of Dermatology, Nanfang Hospital, Southern Medical University, Guangzhou, China, zengkangall25@163.com.
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.
Insights
Small nucleolar RNA host gene 5 (SNHG5) promotes melanoma by inhibiting miR-26a-5p and increasing TRPC3 expression. This finding suggests SNHG5 as a potential therapeutic target for melanoma treatment.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Melanoma is a prevalent skin cancer.
- Small nucleolar RNA host gene 5 (SNHG5) is implicated in various carcinomas.
- The role of SNHG5 in melanoma progression requires detailed investigation.
Purpose of the Study:
- To elucidate the function of SNHG5 in melanoma.
- To explore the underlying molecular mechanisms of SNHG5 in melanoma.
- To assess SNHG5 as a potential therapeutic target for melanoma.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) for gene expression analysis.
- Cell viability, cell cycle, apoptosis, and invasion assays.
- Dual luciferase reporter, RNA immunoprecipitation (RIP), and RNA pull-down assays to determine molecular interactions.
Main Results:
- SNHG5 expression is upregulated in melanoma tissues and cells, correlating with advanced disease.
- SNHG5 acts as a molecular sponge for miR-26a-5p.
- SNHG5 downregulation inhibits melanoma cell proliferation and invasion while promoting apoptosis, effects reversed by miR-26a-5p inhibition.
- miR-26a-5p targets TRPC3, and SNHG5 influences this interaction.
Conclusions:
- SNHG5 promotes melanoma development by downregulating miR-26a-5p and upregulating TRPC3.
- SNHG5 represents a promising novel therapeutic target for melanoma.
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