GP73 regulates autophagy and fibrotic responses in LX-2 cells through the PI3K/AKT/mTOR signaling pathway.

Authors

Shuangyan Luo, Ying He, Lianying Cai, Liu Liu, Yuxu Zhang, Lu Si, Qiuchen Cheng, Yunxiao Liang

Published in

Cytotechnology. Volume 78. Issue 6. Pages 211. Epub Oct 12, 2026.

Abstract

Golgi protein 73 (GP73) has been identified as a potential biomarker for liver diseases. Numerous studies have consistently shown that GP73 expression is significantly elevated in the serum of patients suffering from various types of liver injury. Nevertheless, the underlying regulatory mechanisms by which GP73 contributes to liver fibrosis remain largely undefined. A liver fibrosis model was established by treating LX-2 cells with TGF-β1 for 24 h. LX-2 cells were subsequently cultured and subjected to various treatments, including transfection with plasmids (sh-NC, sh-GP73, oe-GP73) and administration of inhibitors (3-MA and LY294002). Western blot analysis was conducted to quantify protein levels of GP73, fibrosis markers, autophagy-related proteins, and components of the PI3K/AKT/mTOR signaling pathway. Quantitative PCR (qPCR) was utilized to measure GP73 mRNA expression across different samples. Additionally, immunofluorescence assays were performed to evaluate autophagic activity in LX-2 cells. Both mRNA and protein levels of GP73 in LX-2 cells were upregulated following TGF-β1 induction. Activation of the PI3K/AKT/mTOR pathway, as evidenced by increased phosphorylation of PI3K, AKT, and mTOR, along with enhanced autophagy, was observed upon treatment with TGF-β1 or GP73 overexpression. Conversely, silencing GP73 mitigated TGF-β1-induced fibrotic responses. Furthermore, inhibition of the PI3K/AKT/mTOR signaling axis using LY294002 alleviated GP73-mediated suppression of autophagy. The findings suggest that GP73 is associated with autophagy-related changes and fibrotic responses in LX-2 cells, potentially involving modulation of the PI3K/AKT/mTOR signaling pathway.

PMID:
42871167
Bibliographic data and abstract were imported from PubMed on 14 Oct 2026.

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