miR-338-3p targets WAPL to suppress proliferation and invasion in cervical cancer cells: experimental insights

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OBJECTIVE: This study aimed to elucidate the role of miR-338-3p in cervical cancer, focusing on its regulatory effect on the WAPL (wings apart-like homolog) gene and the consequent influence on the behavior of cervical carcinoma cells. MATERIALS AND METHODS: Bioinformatic analysis identified a potential miR-338-3p binding site in the WAPL 3' untranslated region (3'UTR). This interaction was confirmed using a dual-luciferase reporter assay. The effects of miR-338-3p overexpression on the proliferation, apoptosis, cell cycle, and invasion of cervical cancer cells were subsequently evaluated. RESULTS: WAPL transcript levels were elevated in cervical cancer tissues compared with normal controls (P < 0.05). The GV369/miR-338-3p construct was successfully generated, and qRT-PCR confirmed robust upregulation of miR-338-3p expression in HeLa and CaSKi cells. Dual-luciferase assays verified that miR-338-3p directly binds to the 5'-AUGCUGG-3' sequence within the WAPL 3'UTR, leading to reduced luciferase activity (0.59 ± 0.01 vs 1.00 ± 0.01 and 1.16 ± 0.01, P < 0.001) compared with the negative control and mutant groups. Overexpression of miR-338-3p significantly decreased both mRNA and protein levels of WAPL (P < 0.05). Functionally, miR-338-3p overexpression markedly inhibited the proliferation of HeLa and CaSKi cells (P < 0.001), enhanced apoptosis (P < 0.001), induced cell cycle arrest at the S phase in HeLa and at the G1 phase in CaSKi cells (P < 0.05), and reduced cellular invasion and migration (P < 0.05). CONCLUSIONS: miR-338-3p directly targets WAPL to downregulate its expression, thereby suppressing the proliferative and invasive capacities of cervical cancer cells. These findings provide mechanistic insights into the post-transcriptional regulation of WAPL in cervical cancer.

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