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微电流刺激诱导p53-突变和5-FU抗性乳腺癌的细胞死亡

Tomohito Tanihara¹, Yuya Yoshida¹, Takashi Ogino²

¹Faculty of Pharmaceutical Sciences, Department of Clinical Pharmacokinetics, Kyushu University, Fukuoka, Japan.

The Journal of biological chemistry

|June 26, 2025

概括

微电流刺激 (MCS) 可以诱导p53突变乳腺癌细胞的细胞死亡,克服对5-Fluorouracil (5-FU) 化疗的耐药性. 这种方法显示了提高乳腺癌治疗策略的前景.

科学领域:

在瘤学瘤学.
生物医学工程生物医学工程
分子生物学分子生物学

背景情况:

5-甲 (5-FU) 是乳腺癌的标准化疗,但其有效性受到p53突变的限制,这些突变赋予了耐药性.
在乳腺癌治疗中,p53突变是一个重大挑战,导致治疗效率降低和疾病进展.

研究的目的:

研究微电流刺激 (MCS) 在p53突变乳腺癌细胞中诱导细胞死亡的潜力.
评估MCS与5-FU结合的疗效,以克服乳腺癌模型中的化疗抵抗.

主要方法:

利用p53-突变人类乳腺癌细胞系 (MDA-MB-231,MDA-MB-468) 和携带瘤的小鼠模型.
应用微电流刺激 (30分钟300μA) 并评估其对亡,细胞内离子水平,活性氧物种和基因表达的影响.
评估了MCS和5-FU对瘤生长抑制和细胞死亡的联合作用.

主要成果:

在p53-突变乳腺癌细胞中,MCS诱导了亡,包括那些对5-FU耐药的细胞.
在体内,MCS增强了5-FU的抗瘤作用,降低了对5-FU敏感性降低的小鼠的瘤生长.
由MCS诱导的亡与细胞内Cu2+离子增加,反应性氧物种增加以及亲亡基因的p53-介导的转录上调有关.

结论:

微电流刺激是一种可行的策略,可以在p53-突变乳腺癌细胞中诱导p53-介导的亡.
MCS可以克服5-FU耐药性并增强其抗瘤功效,为乳腺癌提供一种新的治疗方法.
这项研究为开发针对p53突变的创新乳腺癌治疗提供了基础.

关键词:

5 - - 甲酸是一种甲.细胞中的MDA-MB-231细胞.灭症 (apoptosis) 是一种死亡的过程.乳腺癌乳腺癌乳腺癌细胞死亡是细胞死亡.化学电阻是一种化学电阻.流动细胞计量是流动细胞计量的方法.微电流是微电流中的一种.在 p53 里,p53 是一个 p53 的类型.反应性氧物种 (ROS) 是一种反应性氧物种.

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