Prostate cancer (PCa) is the second most common cancer in men worldwide. Protein arginine methyltransferase 7 (PRMT7) expression is associated with tumor growth, as it can drive tumor cell proliferation and promote its invasiveness in several types of cancer. However, its mechanism in PCa remains to be elucidated. In the present study, the function and associated mechanism of PRMT7 in PCa cells were investigated. The relationship between PRMT7 and PCa was analyzed using The Cancer Genome Atlas online database. Tissue chip techniques were used to identify the clinical relevance of PRMT7 expression. PRMT7 expression levels in PCa tissues and cells were verified using reverse transcription-quantitative PCR (RT-qPCR). Cell cycle, migration, proliferation and apoptosis of PC3 and DU145 cells were observed using flow cytometry, Cell Counting Kit-8, wound healing, plate cloning and cell invasion assays. Gene set enrichment analysis and chip expression profiles were used to predict the potential signaling pathway involved in the action of PRMT7 in PCa. First, The Cancer Genome Atlas database, tissue microarray analysis and RT-qPCR revealed that PRMT7 expression was increased in PCa tissues and cells. Furthermore, small interfering RNA-mediated PRMT7 knockdown led to a notable reduction in the proliferation of cells, increased apoptosis, affected the cell cycle and decreased cell migration and invasion. Furthermore, PRMT7 regulated the functions of Yin Yang 1 (YY1), tumor protein p53 (TP53), cyclin D2 (CCND2), CDK6 and retinoblastoma 1 (RB1) in PCa. PRMT7 may promote proliferation, migration and metastasis in PCa cells by regulating the activity of YY1, TP53, CCND2, CDK6 and RB1 in the cell cycle signaling pathway.
Protein arginine methyltransferase 7 regulates the cell cycle and promotes the progression of prostate cancer.
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作者:Wan Hongyuan, Zhou Hangshen, Gui Jiandong, Yang Dongjie, Wang Rong, Ni Jiang, Wu Sheng, Qin Yan, Qi Qiaowei, Zhu Lijie, Feng Ninghan, Mi Yuanyuan
| 期刊: | Oncology Letters | 影响因子: | 2.200 |
| 时间: | 2025 | 起止号: | 2025 Sep 23; 30(6):549 |
| doi: | 10.3892/ol.2025.15295 | ||
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