ArticleWorld journal of surgical oncology2025
miR-338-3p targets WAPL to suppress proliferation and invasion in cervical cancer cells: experimental insights.
Article in World journal of surgical oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveThis 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
methodsBioinformatic 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.
resultsWAPL 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).
conclusionsmiR-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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