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目的 探究真核翻译起始因子eIF家族的eIF1a及eIF1a-like对前列腺癌恶性表型的影响。方法构建过表达eIF1a、eIF1a-like1和eIF1a-like2的RM-1稳转细胞系,Real-timePCR检测过表达情况。使用CCK-8检测细胞活力,Ki-67和Annexin-V/7-AAD检测细胞增殖及凋亡,OPP法评估蛋白合成,并进行小鼠皮下成瘤实验。结果 CCK-8实验显示,过表达eIf1a能显著提高细胞活力(P<0.001),而eIF1a-like2则抑制细胞活力及增殖(P<0.001),Annexin-V/7-AAD及OPP实验显示过表达eIF1a-like2促进细胞凋亡(P<0.05)并抑制蛋白合成(P<0.05)。小鼠成瘤实验显示eIF1a-like2能显著抑制肿瘤重量(P<0.01)和体积(P<0.05)。结论eIF1a-like2可以通过调控前列腺癌细胞增殖、凋亡及蛋白合成等过程抑制肿瘤的发生发展过程。
Abstract:Objective To investigate the effects of eIF1a and its homologs, eIF1a-like1 and eIF1a-like2, on the malignant phenotype of prostate cancer cells. Methods Stable RM-1 cell lines overexpressing eIF1a, eIF1a-like1, and eIF1a-like2 were established. Overexpression efficiency was confirmed by Real-time PCR. Cell viability was assessed using the CCK-8 assay, while cell proliferation and apoptosis were evaluated by Ki-67 staining and Annexin-V/7-AAD double staining, respectively. Protein synthesis was measured using the OPP (O-propargyl-puromycin) assay. In vivo tumor growth was examined using a subcutaneous xenograft model in mice. Results CCK-8 assays demonstrated that overexpression of eIF1a significantly enhanced cell viability (P<0.001), whereas overexpression of eIF1a-like2 markedly suppressed cell viability and proliferation (P<0.001). Annexin-V/7-AAD and OPP assays revealed that eIF1a-like2 overexpression promoted apoptosis (P<0.05) and inhibited protein synthesis (P<0.05). In vivo, eIF1a‑like2 overexpression significantly reduced both tumor weight (P<0.01) and tumor volume (P<0.05) in mouse model. Conclusion eIF1a-like2 suppresses prostate cancer progression by modulating cellular processes such as proliferation, apoptosis, and protein synthesis.
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基本信息:
中图分类号:R737.25
引用信息:
[1]沈莹,孙振江,宁金玲,等.真核翻译起始因子eIF1a对前列腺癌RM-1细胞生物学功能的影响[J].安徽医科大学学报().
基金信息:
国家自然科学基金项目(编号:82300281); 苏州大学附属第一医院博习培育计划(编号:BXQN2025003)
2026-09-03
2026-09-03
2026-09-03