Abstract
BACKGROUND: Cervical cancer poses a significant threat to women's health as a leading gynecological malignancy. Among them, HeLa cells, as a classic model for cervical cancer research, have attracted much attention regarding the regulatory mechanisms of their proliferation, apoptosis, and invasion. Research indicates that microRNAs (miRNAs) are critically involved in tumorigenesis and cancer progression. OBJECTIVE: This study investigates how miR-628-5p influences the proliferation, apoptosis, and invasive potential in cervical cancer-derived HeLa cells. MATERIALS AND METHODS: To start with, we quantified miR-628-5p expression in cervical carcinoma tissue using RT-qPCR, with comparisons made to adjacent normal tissues. HeLa cells derived from cervical cancer were divided into four groups: blank control, non-targeting plasmid control (miR-NC), miR-628-5p overexpression, and miR-628-5p knockdown. We evaluated miR-628-5p expression using RT-qPCR, assessed proliferation via MTT assay, analyzed invasion/migration with Transwell chambers, and quantified apoptosis by flow cytometry. RESULTS: Cervical cancer tissues exhibited significant miR-628-5p downregulation compared to both matched normal tissues and controls. Consistent with tumor findings, miR-628-5p levels in paracervical tissues were significantly reduced relative to normal controls. Meanwhile, Overexpression of miR-628-5p produced statistically significant reductions in cellular viability and metastatic propensity in HeLa cultures, alongside a promotion of apoptosis. miR-628-5p knockdown produced opposite effects, significantly enhancing HeLa cell viability and invasiveness while suppressing apoptosis. CONCLUSION: Cervical cancer exhibits reduced miR-628-5p expression. Functional analyses revealed that miR-628-5p overexpression suppresses cervical cancer cell proliferation and invasion while promoting apoptosis. This study provides the first evidence that miR-628-5p functions as a tumor suppressor in HeLa cells.