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Objective <p>This study aimed to elucidate the role of miR-338-3p in cervical cancer, focusing on its regulatory effect on the <i>WAPL</i> (w<i>ings apart-like homolog</i>) gene and the consequent influence on the behavior of cervical carcinoma cells.</p> Materials and methods <p>Bioinformatic analysis identified a potential miR-338-3p binding site in the <i>WAPL</i> 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.</p> Results <p><i>WAPL</i> transcript levels were elevated in cervical cancer tissues compared with normal controls (<i>P</i> &lt; 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 <i>WAPL</i> 3’UTR, leading to reduced luciferase activity (0.59 ± 0.01 vs 1.00 ± 0.01 and 1.16 ± 0.01, <i>P</i> &lt; 0.001) compared with the negative control and mutant groups. Overexpression of miR-338-3p significantly decreased both mRNA and protein levels of <i>WAPL</i> (<i>P</i> &lt; 0.05). Functionally, miR-338-3p overexpression markedly inhibited the proliferation of HeLa and CaSKi cells (<i>P</i> &lt; 0.001), enhanced apoptosis (<i>P</i> &lt; 0.001), induced cell cycle arrest at the S phase in HeLa and at the G1 phase in CaSKi cells (<i>P</i> &lt; 0.05), and reduced cellular invasion and migration (<i>P</i> &lt; 0.05).</p> Conclusions <p>miR-338-3p directly targets <i>WAPL</i> 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 <i>WAPL</i> in cervical cancer.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月7日

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  • Bo Li,
  • Yuye Fu,
  • Ruoyu Wang,
  • Qian Wang,
  • Li Wang,
  • Wenkang Liu

摘要

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.