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通过基因分析和实验验证,确定MTHFD1L在前列腺癌进展中的作用
Yuan-Chin Tsai1,2, Shu-Pin Huang3,4,5,6, Wei-Chung Cheng7
1Graduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University Taipei 110, Taiwan.
American journal of cancer research
|February 7, 2024
概括
单碳代谢中的基因MTHFD1L的遗传变异与前列腺癌的存活率有关. 增加MTHFD1L表达与侵袭性瘤和不良预后相关,影响细胞周期进展.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 遗传学 是一个遗传学.
背景情况:
- 一碳代谢对癌细胞的增殖至关重要,为核酸合成,表观遗传调节和氧化还原代谢提供单位.
- 单碳代谢在前列腺癌进展中的具体作用尚不清楚.
研究的目的:
- 研究一碳代谢途径中的遗传变异与接受抗雄激素剥夺治疗的前列腺癌患者的临床结果之间的关联.
- 探索MTHFD1L在前列腺癌进展中的功能作用.
主要方法:
- 在630名前列腺癌患者中,考克斯回归分析了14个单碳代谢基因中的130个单核酸多态.
- 使用前列腺癌细胞系的功能研究,包括基因淘汰和RNA测序.
- 对多个数据集进行聚合分析,以评估MTHFD1L表达及其与瘤攻击性和预后的相关性.
主要成果:
- MTHFD1L rs2073190多态性与癌症特异性存活率 (CSS) 有意义地相关.
- 聚合分析显示前列腺癌中MTHFD1L升高调节,与瘤的攻击性和患者预后较差有积极的相关性.
- MTHFD1L knockdown 抑制前列腺癌细胞增殖和殖民地形成,受影响的基因在细胞循环途径中得到丰富.
结论:
- 在MTHFD1L的遗传变异可以作为前列腺癌的预测生物标志物.
- MTHFD1L在前列腺癌的进展中发挥着功能性作用,可能通过细胞循环途径的调节.
- 这些发现提高了对前列腺癌进展背后的遗传机制的理解.
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