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FOXO1 inactivation induces cisplatin resistance in bladder cancer
Hiroki Ide1,2,3, Takuro Goto4,5, Yuki Teramoto4,5
1Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Abstract:
We found that FOXO1-shRNA sublines or FOXO1-positive cells co-treated with a FOXO1 inhibitor were significantly more resistant to cisplatin treatment at pharmacological concentrations, compared with respective control sublines or those with mock treatment. Western blot demonstrated considerable increases in the expression levels of a phosphorylated inactive form of FOXO1 (p-FOXO1) in cisplatin-resistant sublines established by long-term culture with low/increasing doses of cisplatin, compared with respective controls. Immunohistochemistry in surgical specimens from patients with muscle-invasive bladder cancer undergoing cisplatin-based neoadjuvant therapy further showed a strong trend to associate between p-FOXO1 positivity and unfavorable response to chemotherapy.
Insights
FOXO1 inhibition increases resistance to cisplatin chemotherapy in bladder cancer. Elevated phosphorylated FOXO1 (p-FOXO1) levels correlate with poor chemotherapy response in patients, suggesting p-FOXO1 as a potential biomarker.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Cisplatin is a cornerstone chemotherapy for muscle-invasive bladder cancer.
- Mechanisms underlying cisplatin resistance are crucial for improving treatment efficacy.
