Targeting TRIP13 for overcoming anticancer drug resistance (Review)

Abstract

Cancer is one of the greatest dangers to human wellbeing and survival. A key barrier to effective cancer therapy is development of resistance to anti-cancer medications. In cancer cells, the AAA+ ATPase family member thyroid hormone receptor interactor 13 (TRIP13) is key in promoting treatment resistance. Nonetheless, knowledge of the molecular processes underlying TRIP13-based resistance to anticancer therapies is lacking. The present study evaluated the function of TRIP13 expression in anticancer drug resistance and potential methods to overcome this resistance. Additionally, the underlying mechanisms by which TRIP13 promotes resistance to anticancer drugs were explored, including induction of mitotic checkpoint complex surveillance system malfunction, promotion of DNA repair, the enhancement of autophagy and the prevention of immunological clearance. The effects of combination treatment, which include a TRIP13 inhibitor in addition to other inhibitors, were discussed. The present study evaluated the literature on TRIP13 as a possible target and its association with anticancer drug resistance, which may facilitate improvements in current anticancer therapeutic options.

In silico analysis unveiling potential biomarkers in gallbladder carcinogenesis

“…TRIP13 reduces Mad2-induced mitotic delay while lowering TRIP13 worsens Mad2 effects. Decreasing TRIP13 and increasing Mad2 inhibits cell and tumor growth, suggesting TRIP13 inhibition as a potential therapy 13 . NIMA-Related Kinase 2 is critical for centrosome maturation and microtubule dynamics and is essential for cell division and motility 14 .…”