Conclusion
Therefore, miR503HG may regulate the drug resistance of CSCC cells by regulating mir-155/Caspase-3.
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.