Targeting TRIP13 for overcoming anticancer drug resistance (Review)
Liwen Zhao1, Siyu Ye1, Shengnan Jing1
1Institute of Pain Medicine and Special Environmental Medicine, Co‑innovation Center of Neuroregeneration, Nantong University, Nantong, Jiangsu 226019, P.R. China.
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.
Insights
Thyroid hormone receptor interactor 13 (TRIP13) drives cancer drug resistance by disrupting cell division and repair. Inhibiting TRIP13 offers a promising strategy to overcome treatment resistance in cancer therapy.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Cancer remains a major threat to human health, with drug resistance significantly hindering effective treatment.
- Thyroid hormone receptor interactor 13 (TRIP13), an AAA+ ATPase, is implicated in promoting cancer treatment resistance.
- The precise molecular mechanisms of TRIP13-mediated anticancer drug resistance are not fully understood.
Purpose of the Study:
- To investigate the role of TRIP13 expression in anticancer drug resistance.
- To explore potential therapeutic strategies to overcome TRIP13-driven resistance.
- To elucidate the molecular mechanisms by which TRIP13 confers resistance to anticancer drugs.
Main Methods:
- Literature review and analysis of existing studies on TRIP13 function in cancer.
- Exploration of TRIP13's involvement in mitotic checkpoint malfunction, DNA repair, autophagy, and immune evasion.
- Discussion of combination therapies involving TRIP13 inhibitors.
Main Results:
- TRIP13 expression is a key factor in the development of resistance to anticancer medications.
- TRIP13 promotes resistance through mechanisms including mitotic checkpoint malfunction, enhanced DNA repair, increased autophagy, and evasion of immune clearance.
- Combination treatments targeting TRIP13 alongside other inhibitors show potential for overcoming resistance.
Conclusions:
- TRIP13 is a critical mediator of anticancer drug resistance.
- Targeting TRIP13 presents a viable therapeutic strategy to improve cancer treatment outcomes.
- Further research into TRIP13 inhibitors and combination therapies is warranted to enhance current anticancer options.
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