LncRNA SNHG1 acts as a ceRNA for miR-216a-3p to regulate TMBIM6 expression in Esophageal Squamous Cell Cancer

Abstract

Abstract Purpose Esophageal squamous cell cancer (ESCC) represents a prevalent malignancy of the digestive system in humans with poor clinical prognosis. The long noncoding RNA SNHG1 has been implicated in the occurrence and pathogenesis of numerous cancers. The regulatory mechanisms of SNHG1 in ESCC are inadequately defined and warrant further investigation. Methods Fifty patients diagnosed with esophageal squamous cell cancer were enrolled to assess overall survival. qRT-PCR was used to examine SNHG1, miR-216a-3p and TMBIM6 expression on TE-1 and KYSE-150 cells. Cell proliferation, apoptosis, migration, and invasion were evaluated by CCK8, flow cytometry, and Transwell assays, respectively. TMBIM6, Calpain, and Caspase-12 protein levels were assessed using Western blot. The interaction between SNHG1, miR-216a-3p, and TMBIM6 was confirmed by luciferase reporter assay. Results Elevated SNHG1 expression in esophageal squamous cell carcinoma (ESCC) patients predicted negative clinical outcomes. Silencing of SNHG1 significantly inhibited cell proliferation, migration, and invasion while promoting apoptosis in ESCC cells. It was discovered that SNHG1 functions as a competing endogenous RNA (ceRNA) in ESCC cells, modulating TMBIM6 expression through sponging miR-216a-3p. Notably, inhibition of miR-216a-3p or restoration of TMBIM6 reversed the inhibitory effect caused by SNHG1 silencing in ESCC cells. Conclusions Through modulation of the miR-216a-3p/TMBIM6 pathway, SNHG1 promotes the advancement of esophageal squamous cell carcinoma, suggesting its potential as a prognostic biomarker and therapeutic target for this disease.