LncRNA mir503HG regulates the drug resistance of recurrent cervical squamous cell carcinoma cells by regulating miR-155/caspase-3

Abstract

Introduction: The purpose of this study is to investigate the role of long non-coding RNA (lncRNA) miR503 Host Gene (miR503HG) in cervical squamous cell carcinoma (CSCC). Methods: Analysis of TCGA dataset revealed that expression levels of miR503HG in CSCC tissues were over 12 times lower than those in non-tumor tissues, indicating its involvement in CSCC. Results: In this study, we observed that levels of miR503HG in plasma were significantly lower in CSCC patients than in healthy participants. The cisplatin-based treatment further downregulated miR503HG in both patients and CSCC cells. MiR503HG overexpression in CSCC cells led to the suppression of miR-155 and elevation of Caspase-3, acting as the downstream target of miR-155. Cell apoptosis analysis showed that miR503HG and Caspase-3 overexpression led to an increased cell apoptosis rate under Cisplatin treatment. MiR-155 played the opposite role and attenuated the functions of Caspase-3 and miR503HG overexpression. Conclusion: Therefore, miR503HG may regulate the drug resistance of CSCC cells by regulating mir-155/Caspase-3.