TTK 通过调节 Akt/mTOR 轴促进 HER2+乳腺癌细胞的迁移、凋亡和对靶向治疗的耐药性。
TTK promotes HER2 + breast cancer cell migration, apoptosis, and resistance to targeted therapy by modulating the Akt/mTOR axis.
机构信息
Department of Clinical Medicine, Guizhou Medical University, Guiyang, China.
Department of General Surgery, Dejiang County People's Hospital, Tongren, Guizhou, China.
出版信息
J Cancer Res Clin Oncol. 2024 Nov 26;150(12):512. doi: 10.1007/s00432-024-06021-9.
BACKGROUND
HER2 + breast cancer is a malignant neoplasm with a high degree of aggressiveness and therapeutic challenge. In recent years, studies have indicated a strong correlation between TTK and various tumors, though its role in HER2 + BRCA remains unclear.
OBJECTIVES
Studying the biological function of the TTK gene in HER2 + BRCA and its resistance to targeted therapy it provides new ideas for targeted drug research.
METHODS
TTK was knocked down by small interfering RNA transfection, and its biological function in HER2 + BRCA cells was verified, and its mechanism of action was verified by RT-PCR and Western blot.
RESULTS
The study demonstrated that TTK promoted cell proliferation and migration by activating the Akt/mTOR pathway in HER2 + breast cancer and enhanced the drug sensitivity of BRCA cell lines SKBR3 and BT474 to pyrotinib, in addition, knockdown of TTK induced apoptosis and arrested cells in G1 phase.
CONCLUSION
Which implies that TTK is an oncogene in HER2 + BRCA and is a valuable research target.
背景
HER2+乳腺癌是一种侵袭性强、治疗挑战性大的恶性肿瘤。近年来的研究表明，TTK 与多种肿瘤之间存在很强的相关性，但它在 HER2+BRCA 中的作用尚不清楚。
目的
研究 TTK 基因在 HER2+BRCA 中的生物学功能及其对靶向治疗的耐药性，为靶向药物研究提供新的思路。
方法
通过小干扰 RNA 转染敲低 TTK，验证其在 HER2+BRCA 细胞中的生物学功能，并通过 RT-PCR 和 Western blot 验证其作用机制。
结果
研究表明，TTK 通过激活 Akt/mTOR 通路促进 HER2+乳腺癌细胞的增殖和迁移，并增强 BRCA 细胞系 SKBR3 和 BT474 对吡咯替尼的药物敏感性，此外，敲低 TTK 诱导细胞凋亡并将细胞阻滞在 G1 期。
结论
这意味着 TTK 是 HER2+BRCA 中的致癌基因，是一个有价值的研究靶点。
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