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DOI 10.2174/0115680096391591250506064859

Медицинская библиотека · Current cancer drug targets · 2025

MND1 Promotes the Proliferation of Prostate Cancer Cell Via the CCNB1/p53 Signaling Pathway.

Zhao Zhongxiang, Zou Yesong, Lv Qian, Wu Chenxiao, Tang Ke, Dai Fazhong, Feng Jiayao, Lai Hongshen, Lai Wenjie, Qiu Xiaofu

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Аннотация

INTRODUCTION

Prostate cancer (PCa) is one of the most commonly diagnosed cancers in men, with a high global incidence. The Meiotic Nuclear Division 1 (MND1) protein is essential for the repair of DNA double-strand breaks during meiosis, but its role in PCa remains poorly understood. This study aims to explore the function of MND1 in PCa progression and the mechanism involved.

METHODS

RNA-Seq data from the TCGA and GEO databases were analyzed. Kaplan-Meier (KM) method and χ2 test examined the association between MND1 expression, prognosis, and clinical parameters. PCa cell lines (22RV1 and C4-2) were used for functional assays. CCK- 8, EdU, colony formation assay, flow cytometry analysis and xenograft model were used to evaluate the effects of MND1 on PCa cell proliferation in vitro and in vivo.

RESULTS

MND1 expression was significantly upregulated in PCa tissues, particularly in cases with Gleason scores ≥8, and correlated with poorer disease-free survival (DFS) and adverse clinical features. Functionally, elevated MND1 expression promoted PCa cell proliferation both in vitro and in vivo. Mechanistically, MND1 facilitated cell cycle progression from G0/G1 to S phase via activation of the CCNB1/p53 signaling pathway.

CONCLUSION

MND1 promotes prostate cancer progression by facilitating the G0/G1 to S phase transition via the CCNB1/p53 pathway, making it a promising prognostic marker and potential therapeutic target.

Для цитирования: Zhao Zhongxiang, Zou Yesong, Lv Qian, Wu Chenxiao, Tang Ke, Dai Fazhong, Feng Jiayao, Lai Hongshen, Lai Wenjie, Qiu Xiaofu. MND1 Promotes the Proliferation of Prostate Cancer Cell Via the CCNB1/p53 Signaling Pathway.. Current cancer drug targets. 2025. DOI: 10.2174/0115680096391591250506064859.

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