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Updated: Oct 18, 2025

Author Spotlight: Unveiling the Role of TMOD3 in Platinum Resistance and Immune Infiltration in Ovarian Cancer
Published on: August 2, 2024
TTK is a potential therapeutic target for cisplatin-resistant ovarian cancer
Yixuan Liu1,2,3, Keyu Zhu1,2, Xiaolin Guan1,2
1Department of Clinical Laboratory, Fudan University Shanghai Cancer Center, No.270, Dong'An Road, Xuhui District, Shanghai, 200032, China.
Background:
Drug resistance and recurrence are main contributors to the poor prognosis of ovarian cancer. Cisplatin is a platinum compound which is widely used in the treatment of various solid tumors including ovarian cancer. Up to now, the mechanism of cisplatin resistance in ovarian cancer is unclear. Threonine and tyrosine kinase (TTK), an integral part of the spindle assembly checkpoint, may be a potential new target associated with chemotherapy sensitivity.
Results:
TTK was up-regulated in the cisplatin-resistant ovarian cancer cell line. Down-regulation of TTK could recover the sensitivity of cisplatin-resistant ovarian cancer cells to cisplatin treatment. Mechanistically, the PI3K/AKT signaling pathway was activated in cisplatin-resistant cells, and this pathway would be affected by TTK expression. Furthermore, TTK was highly expressed in the tissues of ovarian cancer patients, especially those acquired resistance to cisplatin.
Conclusions:
Our study revealed that TTK may be a promising therapeutic target for cisplatin-resistant ovarian cancer.
Insights
Threonine and tyrosine kinase (TTK) is upregulated in cisplatin-resistant ovarian cancer. Inhibiting TTK may restore chemotherapy sensitivity, offering a new therapeutic target for ovarian cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Ovarian cancer prognosis is poor due to drug resistance and recurrence.
- Cisplatin is a key chemotherapy agent, but resistance mechanisms are unclear.
- Threonine and tyrosine kinase (TTK) is a potential target for chemotherapy sensitivity.
Purpose of the Study:
- Investigate the role of TTK in cisplatin resistance in ovarian cancer.
- Determine if TTK is a viable therapeutic target for resistant ovarian cancer.
Main Methods:
- Compared TTK expression in cisplatin-sensitive and resistant ovarian cancer cell lines.
- Assessed the effect of TTK down-regulation on cisplatin sensitivity.
- Analyzed the PI3K/AKT signaling pathway in relation to TTK expression.
- Examined TTK expression in patient tissues with and without cisplatin resistance.
Main Results:
- TTK expression was significantly higher in cisplatin-resistant ovarian cancer cells.
- Reducing TTK levels restored sensitivity to cisplatin treatment.
- The PI3K/AKT pathway was activated in resistant cells and influenced by TTK.
- High TTK expression correlated with cisplatin resistance in patient tissues.
Conclusions:
- TTK plays a crucial role in cisplatin resistance in ovarian cancer.
- Targeting TTK presents a promising therapeutic strategy for overcoming cisplatin resistance.
- TTK is a potential biomarker for predicting cisplatin resistance in ovarian cancer patients.
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