Targeting protein palmitoylation decreases palmitate‑induced sphere formation of human liver cancer cells.

ABSTRACT: Although non‑alcoholic fatty liver disease (NAFLD) is considered a benign disorder, hepatic steatosis has been proposed to be involved in the tumorigenesis of liver cancer. However, the underlying mechanism for carcinogenesis in fatty liver diseases remains unclear. Cancer stem cells (CSCs) have been hypothesized to serve a key role in tumorigenesis. Tumor formation begins with a subset of heterogeneous cells that share properties with stem cells, such as self‑renewal and undifferentiated properties. Our previous study reported that the saturated fatty acid palmitate (PA) significantly enhanced the CSC properties of the HepG2 human liver cancer cell line; however, its underlying mechanisms are unknown. In the present study, a proteomic approach was used to investigate the palmitoylation of

SUBMITTER: Chong LW 

PROVIDER: S-EPMC7339714 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature