SNHG6 facilitates the epithelial-mesenchymal transition and metastatic potential of esophageal squamous carcinoma through miR-26b-5p/ ITGB1 axis.

Long non-coding RNAs (lncRNAs), such as SNHG6, have been identified as crucial regulators in the progression of various cancers, including esophageal squamous cell carcinoma (ESCC). Although the role of SNHG6 in ESCC is not completely understood, our findings demonstrated that SNHG6 expression is upregulated in ESCC tissues compared to adjacent normal tissues. Furthermore, elevated levels of SNHG6 are significantly correlated with higher TNM stage and poorer clinical prognosis in ESCC patients. Functionally, both in vivo and in vitro experiments have shown that knocking down SNHG6 inhibits proliferation, invasion, and metastasis. Luciferase reporter assays and Ago2-RIP assay confirm that SNHG6 functions as a competing endogenous RNA (ceRNA) by sponging miR-26b-5p to modulate ITGB1 expression in ESCC. Given that ITGB1 is instrumental in EMT and metastasis, we assessed the expression of EMT-related proteins. The findings suggest that miR-26b-5p and reduced ITGB1 expression can reverse the EMT induced by lncRNA SHNG6, as demonstrated through rescue analysis. Overall, this study aims to elucidate the molecular mechanisms through which SNHG6 promotes EMT and metastasis in ESCC, providing a novel theoretical foundation for understanding ESCC progression and identifying new targets for improving outcomes in metastatic ESCC.