TTK promotes HER2 + breast cancer cell migration, apoptosis, and resistance to targeted therapy by modulating the Akt/mTOR axis

Abstract

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.