MYLK4 promotes colorectal cancer progression by regulating lipid metabolism reprogramming via targeting ferroptosis.

ABSTRACT: The advancement of novel pharmaceuticals and targeted therapeutic approaches is considerably obstructed by the insufficient comprehension of the intricate pathophysiology of colorectal cancer (CRC). The therapeutic effectiveness of tyrosine kinase inhibitors (TKI)-based systemic treatment for advanced CRC is limited by medication resistance. Research has revealed that therapeutic strategies aimed at the myosin light chain kinase family member 4 (MYLK4) and its corresponding response element can suppress tumour proliferation and yield significant clinical advantages for cancer patients. This study reveals that MYLK4-mediated lipid metabolic reprogramming confers resistance to TKI-induced ferroptosis in CRC. MYLK4 directly interacts with tripartite motif containing 15 (TRIM15) in a way relia

SUBMITTER: Wang B 

PROVIDER: S-EPMC12874343 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature