NCOA4-mediated ferroptosis conducive to EMT inhibition in colorectal cancer cells was achieved through the PI3K/AKT/mTOR pathway.

ABSTRACT: The link of epithelial-mesenchymal transition (EMT) program with metastasis is well documented. However, the role of ROS in EMT process is self-contradictory. DpdtpA was a dithiocarbamate derivative (an iron chelator) that exhibits excellent growth and wound healing inhibitory effects in colorectal cancer (CRC) cell lines, but the underlying mechanism of action was not fully determined. The present data in this study revealed that the ROS derived from autophagic degradation of ferritin were conducive to EMT repression. Genetically knockdown of NCOA4 promoted expression of mesenchymal characteristics, supporting that NCOA4 involved EMT regulation. In addition, DpdtpA treatment also caused depletion of Gpx4 and xCT, triggering ferroptosis as Erastin acted. The causal relationship analysis de

SUBMITTER: Fu Y 

PROVIDER: S-EPMC12606354 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature