Impacts of LncRNA SNHG25 on the Proliferation, Apoptosis, and Immune Escape of Cervical Cancer Cells by Adjusting miR-195-5p/HMGA1 Axis

This study aims to explore the effects of LncRNA SNHG25 (long non-coding RNA SNHG25) regulating the miR-195-5p/HMGA1 axis on the proliferation, apoptosis and immune escape of cervical cancer cells. The expression levels of LncRNA SNHG25 and miR-195-5p in cervical cancer tissues, adjacent tissues, human cer vical epithelial cells H8 and cervical cancer cells HeLa were detected respectively. HeLa cells were divided into the sh-NC group, the sh-SNHG25 group, the sh-SNHG25+miR-195-5p inhibitor group, the sh-SNHG25+inhibitor NC group, the miR-NC group, the miR-195-5p mimics group, the miR-195-5p mimics+pcDNA group, and the miR 195-5p mimics+HMGA1 group. The expression levels of LncRNA SNHG25, miR-195-5p and HMGA1 mRNA were detected by qRT-PCR method. Cell viability was detected by the CCK-8 assay kit. The colony formation as say was used to detect the proliferation ability. Cell apoptosis was detected by flow cytometry. The wound healing assay was used to detect the migration ability of cells. Cell invasion ability was detected by the Transwell method. The protein expression levels of HMGA1, N-cadherin, E-cadherin and cleaved-caspase 3 were detected by Western blot. The levels of IFN-γ, IL-4 and IL-10 in the supernatant of CD8+ T cells co-cultured with HeLa cells were de tected by ELISA. Dual luciferase reporter assay was applied to verify the targeting relationship between LncRNA SNHG25 and miR-195-5p, and miR-195-5p and HMGA1. The expression of LncRNA SNHG25 was upregulated and the expression of miR-195-5p was downregulated in cervical cancer tissues and HeLa cells. Silencing the ex pression of LncRNA SNHG25 or overexpressing miR-195-5p could significantly reduce the number of HeLa cell clones, the number of invasive cells and the scratch healing rate, as well as the protein expression levels of HMGA1 and N-cadherin, while the apoptosis rate and the protein expression levels of E-cadherin and cleaved-caspase 3 were increased (P<0.05). Inhibition of miR-195-5p or overexpression of HMGA1 could reverse the inhibitory effects of silencing LncRNA SNHG25 or overexpression of miR-195-5p on HeLa cell proliferation, migration, invasion, and epithelial-mesenchymal transition (P<0.05). Dual luciferase reporter gene experiments confirmed that miR-195-5p had targeted relationships with LncRNA SNHG25 and HMGA1, respectively. Silencing LncRNA SNHG25 could inhibit immune escape in HeLa cells by targeting miR-195-5p/HMGA1 axis. The expression of LncRNA SNHG25 is upregulated in cervical cancer tissues and cells. Silencing LncRNA SNHG25 can inhibit HeLa cell proliferation, migration, invasion, and immune escape, and promote HeLa cell apoptosis by upregulating miR-195-5p and down regulating HMGA1.

CSTR: 32200.14.cjcb.2025.11.0018