Choline kinase and miR-32-5p: A crucial interaction promoting apoptosis and delaying wound repair in cervical cancer cells

Abstract

<p>Cervical cancer remains a significant global health challenge, especially in low- and middle-income countries. The elucidation of the molecular pathways underlying the carcinogenesis of cervical cancer is vital to develop targeted therapies. Our study investigates the regulatory effects of miR-32-5p on the choline kinase alpha (<italic>chka</italic>) gene in HeLa cells, a well-established cervical cancer cell line. Choline kinase alpha is recognized for its role in phosphatidylcholine biosynthesis, which is crucial for cell membrane formation, and is implicated in the oncogenic transformation of cells. Utilizing a combination of in silico prediction, luciferase assays, RT-qPCR, and Western blot analyses, we demonstrated that miR-32-5p directly targets the 3′ untranslated region (3′UTR) of <italic>chka</italic> mRNA, leading to a significant downregulation of <italic>chka</italic> expression. Our results demonstrate that miR-32-5p significantly downregulates <italic>chka</italic> at both the mRNA and protein levels, thus leading to decreased cellular proliferation and increased apoptosis. This was further confirmed by a cell cycle analysis, which showed a notable arrest in the G0/G1 phase. Additionally, scratch assays indicated a reduced migratory capacity in miR-32-5p-transfected cells, suggesting the potential anti-metastatic properties of miR-32-5p. These findings highlight the therapeutic potential of miR-32-5p as a biomarker and a target in cervical cancer treatment strategies. By modulating <italic>chka</italic> expression, miR-32-5p could serve as a novel approach to curb the progression and spread of cervical cancer, thus offering a promising avenue for future research and clinical applications. This study contributes to the growing understanding of miRNA-mediated gene regulation in cancer biology and underscores the importance of targeted genetic research in the development of cancer therapeutics.</p>