miR-125a attenuates the malignant biological behaviors of cervical squamous cell carcinoma cells through Rad51

Bioengineered. 2022 Apr;13(4):8503-8514. doi: 10.1080/21655979.2022.2051827.

Abstract

Cervical squamous cell carcinoma (CSCC), the most common cervical malignancy, is more likely to invade and metastasize than other cervical cancers. miR-125a, a tumor suppressor gene, has been confirmed to be associated with cancer metastasis. However, the role of miR-125a in CSCC and the underlying mechanism are unknown. miR-125a expression was confirmed by real-time quantitative PCR (RT-qPCR), and the Rad51 expression level was measured by western blotting analysis. CSCC cell proliferation, migration and invasion were assessed with functional assays, including CCK-8, colony formation, wound healing and Transwell assays. Our data confirmed that miR-125a is expressed at low levels in CSCC tissues and cells. Functionally, the overexpression of miR-125a greatly prevented the proliferation, migration and invasion of CSCC cells, and the inhibition of miR-125a expression strongly enhanced these behaviors in CSCC cells. Moreover, the expression of Rad51, a miR-125a target gene, greatly reversed the miR-125-mediated inhibition of CSCC cell proliferation, migration and invasion. In addition, we discovered that miR-125a downregulated the levels of phosphorylated PI3K, AKT and mTOR through Rad51 in CSCC cells. miR-125a, a tumor suppressor, can attenuate the malignant behaviors of CSCC cells by targeting Rad51. Therefore, the miR-125a/Rad51 axis might be a target for CSCC therapy.

Keywords: Cervical squamous carcinoma; PI3K/Akt; Rad51; microRNA-125a.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Carcinoma, Squamous Cell* / genetics
  • Cell Line, Tumor
  • Cell Movement / genetics
  • Cell Proliferation / genetics
  • Female
  • Humans
  • MicroRNAs* / genetics
  • Rad51 Recombinase* / genetics
  • Uterine Cervical Neoplasms* / genetics

Substances

  • MIRN125 microRNA, human
  • MicroRNAs
  • RAD51 protein, human
  • Rad51 Recombinase

Grants and funding

This work was supported by the Natural Science Foundation of Fujian Province (2019J01146) and the Longyan Science and Technology Planning Project (2020LYF9014).