86P - Functional impact of miR-205-5p on cervical cancer cell behavior and chemotherapy response

Background

MicroRNAs (miRNAs) regulate cancer pathophysiology, promising to diagnose and treat cervical cancer. Recent studies have indicated that miR-205-5p could be a promising biomarker for distinguishing CIN 3 lesions. This study aims to evaluate the impact of miR-205-5p on cervical cancer cells and its interaction with cisplatin-induced apoptosis.

Methods

The expression of MicroRNA-205-5p was assessed using quantitative PCR (qPCR) in a panel of cervical cancer cell lines, compared to the non-tumorigenic epithelial cell line HaCaT. Cells were transfected with anti-miR-205-5p and evaluated for proliferation, migration, invasion, and apoptosis. Apoptosis was assessed in CaSki cells after transfection with anti-miRNA alone or in combination with cisplatin (IC50: 1.05 μg/mL). The transcriptional profile characterization between cells receiving miRNA inhibition versus the negative control was performed using the nCounter PanCancer Progression panel (NanoString Technologies). Subsequently, in silico analyses were conducted to validate potential miR-205-5p targets.

Results

Although anti-miR-205-5p reduced proliferation, migration, and invasion, apoptosis suppression was negligible. However, combining miR-205-5p inhibition with cisplatin significantly increased late apoptosis in CaSki cells, indicating an additive effect. Transcriptional profiling using NanoString revealed three upregulated genes following miR-205-5p inhibition: MGP, MMRN2, and FXYD6, the latter predicted as a target of miR-205-5p. FXYD6 may influence ion transport pathways and HOX gene activation during tumor differentiation, suggesting its role in cervical cancer progression.

Conclusions

This study offers valuable insights into the functional role of miR-205-5p in cervical cancer progression and its potential implications as a biomarker for disease identification and monitoring. The findings suggest a regulatory axis involving miR-205-5p and FXYD6 during cervical cancer progression, as well as a potential mediator biomarker response to cisplatin in cervical cancer cells.

Editorial acknowledgement

Clinical trial identification

Legal entity responsible for the study

The authors.

Funding

Has not received any funding.

Disclosure

All authors have declared no conflicts of interest.