ArticleCurrent cancer drug targets2025
MND1 Promotes the Proliferation of Prostate Cancer Cell
Article in Current cancer drug targets, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- MND1 reduces breast cancer chemosensitivity by promoting RAD51-mediated homologous recombination repair.Cell death & disease · 2026Article
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Authors and funding
10 authors.
Funding
Abstract
introductionProstate 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.
methodsRNA-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
resultsMND1 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
conclusionMND1 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.
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Registered trials
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