在乳腺癌中,PER1通过调节MEK5/ERK5信号通路,作为瘤抑制剂
Yinfeng Liu1, Dandan Yang2, Zihang Xu1
1Breast Disease Diagnosis and Treatment Center, The First Hospital of Qinhuangdao, Qinhuangdao, Hebei, People's Republic of China.
International journal of general medicine
|August 14, 2025
概括
周期昼夜蛋白同源1 (PER1) 作为乳腺癌 (BC) 的瘤抑制剂. 低PER1表达与生存率低下和转移率增加相关,而其对MEK5/ERK5通路的调节表明了治疗潜力.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 循环节律 循环节律 循环节律
背景情况:
- 乳腺癌 (BC) 是全球领先的恶性瘤.
- 周期昼夜蛋白质同位素1 (PER1) 是分子时钟振荡的组成部分.
- 了解PER1在BC进展中的作用对于治疗开发至关重要.
研究的目的:
- 研究PER1表达和乳腺癌的临床结果之间的关联.
- 确定PER1对乳腺癌瘤发育和进展的影响.
- 探索PER1在BC中的功能背后的分子机制.
主要方法:
- 免疫组织化学用于评估172个BC组织和30个正常样本中的PER1表达.
- 西方涂抹分析了MEK/ERK通路中的关键蛋白质和酸化水平.
- 用ERK5抑制剂XMD17-109对PER1操纵的BC细胞系 (BT-549,MCF-7) 进行了应用.
主要成果:
- 低PER1表达与增加淋巴结转移和血管血栓形成 (P<0.05) 有关.
- 低PER1的患者的整体存活率和无复发存活率明显降低 (P<0.05).
- PER1调节了ERK5酸化,其对扩散和入侵的淘汰效应被ERK5抑制剂抵消.
结论:
- PER1在乳腺癌中发挥了抗瘤作用.
- PER1通过MEK5/ERK5信号通路调节乳腺癌的进展.
- 针对PER1-MEK5/ERK5轴可能为BC提供一种新的治疗策略.
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