通过P53通路,CAPG干扰会诱导结直肠癌细胞的亡和铁亡
Yingying Zhao1, Rui Ma1, Chuyue Wang1
1Guangdong Institute of Gastroenterology, Guangzhou, China; Guangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Disease, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Molecular and cellular probes
|July 19, 2023
概括
覆盖性动蛋白 (CAPG) 在结直肠癌 (CRC) 中过度表达,促进瘤生长. 抑制CAPG会阻止CRC细胞的增殖并触发细胞死亡,这表明CAPG是CRC的一个有希望的治疗点.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 生物化学 生物化学
背景情况:
- 大肠直肠癌 (CRC) 的发病率和死亡率很高.
- 对于许多患者来说,CRC的现有治疗方法不足.
- 覆盖性动因蛋白 (CAPG) 在动因动态中发挥作用.
研究的目的:
- 调查Capping Actin Protein (CAPG) 作为结直肠癌 (CRC) 的新型治疗标.
- 确定CAPG在CRC进展和患者预后中的作用.
主要方法:
- 利用生物信息分析 (UALCAN) 进行基因表达特征分析.
- 通过CCK-8测定和流细胞计量评估细胞增殖,细胞循环,细胞亡和铁亡.
- 通过小鼠模型在体内评估瘤发生,并通过RNA测序确定差异表达的基因/途径.
主要成果:
- 在CRC组织中,CAPG显著过度表达,与整体存活率差相关.
- 在体外和体内,CAPG倒置抑制了CRC细胞的增殖.
- CAPG干扰阻断了G1阶段的细胞周期,并通过P53通路诱导了细胞亡和铁亡.
结论:
- 在CRC患者中CAPG水平升高表明预后较差.
- 通过抑制P53通路,CAPG促进CRC增殖,同时抑制亡和铁亡.
- CAPG代表了改善CRC预后和治疗结果的潜在治疗目标.
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