Regulation of cisplatin resistance in bladder cancer by epigenetic mechanisms

Bladder cancer is one of the most common malignancies in the world. Cisplatin is one of the most potent and widely used anticancer drugs and has been employed in several malignancies. Cisplatin-based combination chemotherapies have become important adjuvant therapies for bladder cancer patients. Cisplatin-based treatment often results in the development of chemoresistance, leading to therapeutic failure and limiting its application and effectiveness in bladder cancer. To develop improved and more effective cancer therapy, research has been conducted to elucidate the underlying mechanism of cisplatin resistance. Epigenetic modifi-cations have been demonstrated involved in drug resistance to chemotherapy, and epigenetic biomarkers, such as urine tumor DNA methylation assay, have been applied in patients screening or monitoring. Here, we provide a systematic description of epigenetic mechanisms, including DNA methylation, noncoding RNA regulation, m6A modification and posttranslational modifications, related to cisplatin resistance in bladder cancer.

Automated summary

Bladder cancer is a common malignancy worldwide, and cisplatin-based combination chemotherapies have become important adjuvant therapies. However, the development of chemoresistance limits the effectiveness of cisplatin treatment. Epigenetic modifications, such as DNA methylation and noncoding RNA regulation, have been found to be involved in cisplatin resistance, and epigenetic biomarkers have been applied for patient screening and monitoring.