The study presents compelling evidence of the miR-146b-5p/FDFT1 axis modulating cisplatin sensitivity in bladder cancer by altering the cholesterol biosynthesis pathway and activating Ras and Rho signaling. However, Figure 6 focuses on gene expression and cholesterol level changes without directly demonstrating how these modifications impact cisplatin resistance mechanistically. Were functional assays, such as Ras and Rho activation studies or cholesterol flux analyses, performed to confirm their involvement in driving resistance? Additionally, the omission of direct protein-level validation for key pathway components limits the ability to draw definitive conclusions about the molecular mechanisms. Could the authors address these gaps to strengthen the study’s impact?
