Yinhuai Wang

Abstract Cisplatin-based combination therapy remains the primary treatment modality for patients with advanced bladder cancer (BCa); however, the emergence of drug resistance severely restricts clinical benefits. The molecular mechanisms underlying chemoresistance remain incompletely understood. By integrating single-cell transcriptomics with in vitro and in vivo experiments, we revealed that cholesterol metabolism was significantly hyperactivated in cisplatin-resistant BCa tissues.

Introduction Bladder cancer (BLCA) is a prevalent and deadly form of urinary cancer, and there is a need for effective therapies, particularly for muscle-invasive bladder cancer (MIBC). Cell cycle inhibitors show promise in restoring control of the cell cycle in BLCA cells, but their clinical prognosis evaluation is limited. Methods Transcriptome and scRNA-seq data were collected from the Cancer Genome Atlas Program (TCGA)-BLCA and GSE190888 cohort, respectively.