MiR-4327 targets TP53 to promote cervical cancer cell proliferation

Abstract

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.

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