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

BackgroundHER2 + 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.ObjectivesStudying the biological function of the TTK gene in HER2 + BRCA and its resistance to targeted therapy it provides new ideas for targeted drug research.MethodsTTK 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.ResultsThe 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.ConclusionWhich implies that TTK is an oncogene in HER2 + BRCA and is a valuable research target.