黄素通过上调 miR-483-3p 和抑制 UBE2C 来抑制前列腺癌
Wenji Li1,2,3, Fujun Wang1,2,3, Xiaoxiang Wang4
1Institute of Translational Medicine, Medical College, Yangzhou University, Yangzhou, Jiangsu, PR China.
Journal of biochemical and molecular toxicology
|February 13, 2024
概括
黄素 (CUR) 通过抑制细胞增殖和增强细胞亡来抑制前列腺癌 (PCa) 的进展. 它针对miR-483-3p/UBE2C通路,为PCa诊断和治疗提供潜在的新生物标志物.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 前列腺癌 (PCa) 是老年男性普遍存在的恶性瘤,黄素 (CUR) 显示出潜在的抗癌作用.
- 在PCa中CUR的精确药理机制仍然不完全理解.
- 乌比奎丁结合酶E2C (UBE2C) 在PCa上调节,与癌症进展有关.
研究的目的:
- 阐明CUR抗前列腺癌效应背后的分子机制.
- 调查miR-483-3p/UBE2C轴在CUR对PCa的作用中的作用.
- 探索PCa.的潜在诊断和治疗点.
主要方法:
- 使用PCa细胞模型进行体外研究,以评估CUR对增殖和亡的影响.
- 在活体外移植小鼠模型中,评估CUR对瘤生长的影响.
- 在CUR治疗后分析UBE2C和miR-483-3p表达水平.
- 通过siRNA介导的UBE2C和双化酶记者基因测定来确认分子相互作用.
主要成果:
- 在剂量和时间上,CUR抑制了PCa细胞增殖并诱导了细胞亡.
- 在体内,CUR的使用显著降低了异种移植瘤的生长.
- 在PCa细胞中,CUR治疗降低了UBE2C表达,并增加了miR-483-3p表达.
- 击败UBE2C抑制了PCa细胞的增殖,迁移和入侵,miR-483-3p直接与UBE2C结合.
结论:
- 通过调节miR-483-3p/UBE2C信号通路,CUR在前列腺癌中发挥抗瘤作用.
- 这些发现突出了miR-483-3p/UBE2C轴作为CUR疗效的关键调解器.
- 这项研究表明UBE2C和miR-483-3p是PCa诊断和治疗干预的潜在新生物标志物.
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