A Novel Mechanism of the p53 Isoform Δ40p53α in Regulating Collagen III Expression in TGFβ1-Induced LX-2 Human Hepatic Stellate Cells.

ABSTRACT: Injured liver cells undergoing chronic wound healing produce excessive amounts of extracellular matrix (ECM) components, such as collagen and fibronectin, leading to fibrosis. This process is largely mediated by transforming growth factor-β (TGFβ) signaling, which intersects with the tumor suppressor p53 pathway. However, the roles of specific p53 isoforms in this interaction remain unclear. In this study, we report the involvement of the Δ40p53α isoform, an N-terminal truncated variant of p53, in regulating ECM gene expression in TGFβ1-activated LX-2 human hepatic stellate cells. RT-PCR analysis of cirrhotic liver tissues revealed clinically relevant increases in Δ40p53 expression. Knockdown of Δ40p53 using antisense oligonucleotides in LX-2 cells attenuated TGFβ1-induced activation and s

SUBMITTER: Lee SY 

PROVIDER: S-EPMC11999059 | biostudies-literature | 2025 Apr

REPOSITORIES: biostudies-literature