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<p>Cervical cancer is a leading cause of female malignancy worldwide. While microRNA-4327 (miR-4327) has been implicated as a potential oncogene, its functional role and molecular mechanisms in cervical cancer pathogenesis remain unclear. This study aimed to determine the oncogenic function of miR-4327 and elucidate its downstream regulatory mechanism in cervical cancer pathogenesis. We measured miR-4327 expression in clinical cervical cancer tissues and cell lines using quantitative real-time PCR (qRT-PCR). We then assessed its effects on proliferation, migration, invasion, and cell cycle progression through functional assays including cell counting kit-8 (CCK-8), colony formation, transwell, and flow cytometry. To evaluate tumor growth in vivo, we established a xenograft model in non-obese diabetic (NOD)-severe combined immune-deficient (scid) mice. Using bioinformatic analysis and luciferase reporter assays, we identified TP53 as a direct target of miR-4327 and further validated this regulatory relationship with gain- and loss-of-function experiments. We found that miR-4327 was significantly upregulated in cervical cancer and promoted malignant phenotypes such as proliferation, migration, invasion, and cell cycle progression in vitro. Consistent with this, overexpression of miR-4327 accelerated tumor growth in vivo. Mechanistically, we confirmed TP53 as a direct functional target of miR-4327. Knocking down TP53 phenocopied the oncogenic effects of miR-4327, while restoring TP53 expression rescued the tumor-promoting effects mediated by miR-4327. These findings reveal a novel miR-4327/TP53 regulatory axis and nominate miR-4327 as a potential therapeutic target for intervention.</p>

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MiR-4327 targets TP53 to promote cervical cancer cell proliferation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月11日

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  • Mei-Lin Chen,
  • Chen-Yang Chu,
  • Feng-Xian Zhang,
  • Li-Pei Zhang,
  • Ying Yang,
  • Bai-Zhao Peng,
  • Chuang-Hai Wu,
  • Xiao-Mei Chen,
  • Yan-Ting You,
  • Bing-Ying Rong,
  • Hiu Yee Kwan,
  • Xiao-Shan Zhao,
  • Yan-Yan Liu

摘要

Cervical cancer is a leading cause of female malignancy worldwide. While microRNA-4327 (miR-4327) has been implicated as a potential oncogene, its functional role and molecular mechanisms in cervical cancer pathogenesis remain unclear. This study aimed to determine the oncogenic function of miR-4327 and elucidate its downstream regulatory mechanism in cervical cancer pathogenesis. We measured miR-4327 expression in clinical cervical cancer tissues and cell lines using quantitative real-time PCR (qRT-PCR). We then assessed its effects on proliferation, migration, invasion, and cell cycle progression through functional assays including cell counting kit-8 (CCK-8), colony formation, transwell, and flow cytometry. To evaluate tumor growth in vivo, we established a xenograft model in non-obese diabetic (NOD)-severe combined immune-deficient (scid) mice. Using bioinformatic analysis and luciferase reporter assays, we identified TP53 as a direct target of miR-4327 and further validated this regulatory relationship with gain- and loss-of-function experiments. We found that miR-4327 was significantly upregulated in cervical cancer and promoted malignant phenotypes such as proliferation, migration, invasion, and cell cycle progression in vitro. Consistent with this, overexpression of miR-4327 accelerated tumor growth in vivo. Mechanistically, we confirmed TP53 as a direct functional target of miR-4327. Knocking down TP53 phenocopied the oncogenic effects of miR-4327, while restoring TP53 expression rescued the tumor-promoting effects mediated by miR-4327. These findings reveal a novel miR-4327/TP53 regulatory axis and nominate miR-4327 as a potential therapeutic target for intervention.