LncRNA SNHG5 promotes the invasion and proliferation of oropharyngeal squamous cell carcinoma by regulating the miR-21/PTEN signaling pathway.

Abstract

Objective: To delineate the functional role of long non-coding RNA (LncRNA) SNHG5 in oropharyngeal squamous cell carcinoma (OPSCC).

Methods: The expression of LncRNA SNHG5 in paired tumor/adjacent tissues and cell lines (HN6 vs. HIOEC) were detected, and the relationship between LncRNA SNHG5 expression in cancer tissues and the clinicopathological characteristics and prognosis of patients was analyzed. The functional characterization including proliferation, expression of LncRNA SNHG5, miR-21, PTEN, VEGF, MMP-9, cell invasion, as well as cell apoptosis were detected in siRNA-mediated SNHG5 knockdown in HN6 cells.

Results: Tumor tissues exhibited higher SNHG5 expression versus adjacent mucosa (P<0.001). Elevated SNHG5 positively correlated with advanced TNM staging, lymph node metastasis, and poor differentiation (P<0.05). Patients with high SNHG5 showed significantly reduced 5-year overall survival (P=0.035). SNHG5 silencing decreased proliferation and invasion capacity, while increasing apoptosis. Mechanistically, SNHG5 knockdown downregulated oncogenic miR-2, VEGF, and MMP-9, while restoring tumor-suppressive PTEN expression.

Conclusion: Our findings suggest SNHG5 is a master oncogenic regulator in OPSCC that mechanistically promotes tumor progression via miR-21/PTEN pathway activation. The strong association between SNHG5 overexpression and adverse clinicopathological features, coupled with its prognostic independence, positions this lncRNA as a promising therapeutic target and molecular stratification biomarker.