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

IF 2.3 4区 医学 Q3 ONCOLOGY
Zhongxiang Zhao, Yesong Zou, Qian Lv, Chenxiao Wu, Ke Tang, Fazhong Dai, Jiayao Feng, Hongshen Lai, Wenjie Lai, Xiaofu Qiu
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引用次数: 0

Abstract

Introduction: Prostate cancer (PCa) is one of the most commonly diagnosed can-cers 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 re-mains 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.

MND1通过CCNB1/p53信号通路促进前列腺癌细胞增殖
简介:前列腺癌(PCa)是男性最常见的癌症之一,全球发病率很高。减数分裂核分裂1 (MND1)蛋白对减数分裂期间DNA双链断裂的修复至关重要,但其在PCa中的作用仍然知之甚少。本研究旨在探讨MND1在前列腺癌进展中的作用及其机制。方法:对TCGA和GEO数据库的RNA-Seq数据进行分析。Kaplan-Meier (KM)法和χ2检验检验MND1表达与预后及临床参数的相关性。用PCa细胞系(22RV1和C4-2)进行功能检测。采用CCK-8、EdU、集落形成法、流式细胞术和异种移植模型评价MND1对PCa细胞体外和体内增殖的影响。结果:MND1表达在PCa组织中显著上调,特别是在Gleason评分≥8的病例中,并且与较差的无病生存期(DFS)和不良临床特征相关。在功能上,MND1表达的升高促进了体内和体外PCa细胞的增殖。机制上,MND1通过激活CCNB1/p53信号通路促进细胞周期从G0/G1期向S期进展。结论:MND1通过CCNB1/p53通路促进前列腺癌的G0/G1期向S期转变,从而促进前列腺癌的进展,是一个有前景的预后标志物和潜在的治疗靶点。
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来源期刊
Current cancer drug targets
Current cancer drug targets 医学-肿瘤学
CiteScore
5.40
自引率
0.00%
发文量
105
审稿时长
1 months
期刊介绍: Current Cancer Drug Targets aims to cover all the latest and outstanding developments on the medicinal chemistry, pharmacology, molecular biology, genomics and biochemistry of contemporary molecular drug targets involved in cancer, e.g. disease specific proteins, receptors, enzymes and genes. Current Cancer Drug Targets publishes original research articles, letters, reviews / mini-reviews, drug clinical trial studies and guest edited thematic issues written by leaders in the field covering a range of current topics on drug targets involved in cancer. As the discovery, identification, characterization and validation of novel human drug targets for anti-cancer drug discovery continues to grow; this journal has become essential reading for all pharmaceutical scientists involved in drug discovery and development.
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