MicroRNA-146b-5p/FDFT1 mediates cisplatin sensitivity in bladder cancer by redirecting cholesterol biosynthesis to the non-sterol branch.

Chemotherapy against muscle-invasive bladder cancer is increasingly challenged by the prevalence of chemoresistance. The cholesterol biosynthesis pathway has garnered attention in studies of chemoresistance, but conflicting clinical and molecular findings necessitate a clearer understanding of its underlying mechanisms. Recently, we identified farnesyl-diphosphate farnesyltransferase 1 (FDFT1)-the first specific gene in this pathway-as a tumor suppressor and chemoresistance modulator.

Spectroscopic diagnosis and metabolite characterization of cisplatin resistance regulated by FDFT1 in bladder cancer tissue.

As is the case for most solid tumours, chemotherapy remains the backbone in the management of metastatic disease. However, the occurrence of chemotherapy resistance is a cause to worry, especially in bladder cancer. Extensive evidence indicates molecular changes in bladder cancer cells to be the underlying cause of chemotherapy resistance, including the reduced expression of farnesyl-diphosphate farnesyltransferase 1 (FDFT1) - a gene involved in cholesterol biosynthesis.

The role of tumour microenvironment-driven miRNAs in the chemoresistance of muscle-invasive bladder cancer-a review.

Successful treatment for muscle-invasive bladder cancer is challenged by the ability of cancer cells to resist chemotherapy. While enormous progress has been made toward understanding the divergent molecular mechanisms underlying chemoresistance, the heterogenous interplay between the bladder tumour and its microenvironment presents significant challenges in comprehending the occurrence of chemoresistance. The last decade has seen exponential interest in the exploration of microRNA (miRNA) as a tool in the management of chemoresistance.