LncRNA SNHG1 promotes epithelial-mesenchymal transition and progression in clear cell renal cell carcinoma via the miR-200a/ZEB1 axis.

This study aimed to investigate whether long non-coding RNA SNHG1 (LncRNA SNHG1) affects the progression of clear cell renal cell carcinoma (ccRCC) by competitively binding to miR-200a to regulate the ZEB1/epithelial-mesenchymal transition (EMT) pathway. SNHG1 expression was knocked down in ccRCC cell lines. CCK-8 assay, scratch wound healing assay, Transwell assay, and flow cytometry were employed to detect cell proliferation, migration, invasion, and apoptosis. Bioinformatics analysis, dual-luciferase reporter assay, and RNA immunoprecipitation assay were used to validate the targeting relationship between SNHG1 and miR-200a. qPCR and Western blot techniques, combined with miR-200a inhibitors, were utilized to explore the effects of SNHG1 and miR-200a on malignant phenotypes of tumor cells and the expression of EMT-related proteins. SNHG1 knockdown significantly inhibited ccRCC cell proliferation, migration, and invasion, while promoting apoptosis. Experiments confirmed that SNHG1 functions as a competitive endogenous RNA to adsorb miR-200a. Inhibition of miR-200a reversed the inhibitory effect of SNHG1 knockdown on the malignant phenotype of tumor cells and the expression of ZEB1 and EMT-related marker, including vimentin, N-cadherin and E-cadherin. SNHG1 competitively binds to miR-200a, thereby relieving its inhibitory effect on the downstream target gene ZEB1, subsequently inducing EMT and promoting ccRCC progression.