ArticleHepatology (Baltimore, Md.)2014
Liver-specific knockout of GRP94 in mice disrupts cell adhesion, activates liver progenitor cells, and accelerates liver tumorigenesis.
Article in Hepatology (Baltimore, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 67 citations in OpenAlex.
- Nuclear pore complex protein RANBP2 and related SUMOylation in solid malignancies.Genes & diseases · 2025Review
- Liver oval cells in response to HDAC1 inhibitor trichostatin A: immunohistochemical characterization using OV-6 hepatic expression.Anatomy & cell biology · 2025Article
- Progress of mitochondrial and endoplasmic reticulum-associated signaling and its regulation of chronic liver disease by Chinese medicine.World journal of hepatology · 2024Article
- Review
- Review
- Cellular gp96 upregulates AFP expression by blocking NR5A2 SUMOylation and ubiquitination in hepatocellular carcinoma.Journal of molecular cell biology · 2023Article
- GRP78/BiP alleviates oxLDL-induced hepatotoxicity in familial hypercholesterolemia caused by missense variants of LDLR in a HepG2 cellular model.Lipids in health and disease · 2023Article
- gp96 Expression in Gliomas and Its Association with Tumor Malignancy andJournal of oncology · 2022Article
- Review
- Cell Surface GRP94 as a Novel Emerging Therapeutic Target for Monoclonal Antibody Cancer Therapy.Cells · 2021Review
- The loss-of-function PCSK9Q152H variant increases ER chaperones GRP78 and GRP94 and protects against liver injury.The Journal of clinical investigation · 2021Article
- Molecular Chaperone GRP94/GP96 in Cancers: Oncogenesis and Therapeutic Target.Frontiers in oncology · 2021Review
- Coordination of the unfolded protein response during hepatic steatosis identifies CHOP as a specific regulator of hepatocyte ballooning.Cell stress & chaperones · 2020Article
- Oncogenic driver genes and tumor microenvironment determine the type of liver cancer.Cell death & disease · 2020Review
- LncRNA GOLGA2P10 is induced by PERK/ATF4/CHOP signaling and protects tumor cells from ER stress-induced apoptosis by regulating Bcl-2 family members.Cell death & disease · 2020Article
- Overexpression of molecule GRP94 favors tumor progression in lung adenocarcinoma by interaction with regulatory T cells.Thoracic cancer · 2020Article
- Differential regulation of the unfolded protein response in outbred deer mice and susceptibility to metabolic disease.Disease models & mechanisms · 2019Article
- Glucose-Regulated Protein 94 Modulates the Response of Osteosarcoma to Chemotherapy.Disease markers · 2019Article
- Loss-of-function PCSK9 mutants evade the unfolded protein response sensor GRP78 and fail to induce endoplasmic reticulum stress when retained.The Journal of biological chemistry · 2018Article
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7 authors at 2 institutions in 1 country.
Funding
Abstract
unlabelledLiver cancer is one of the most common solid tumors, with poor prognosis and high mortality. Mutation or deletion of the tumor suppressor phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is strongly correlated with human liver cancer. Glucose-regulated protein 94 (GRP94) is a major endoplasmic reticulum (ER) chaperone protein, but its in vivo function is still emerging. To study the role of GRP94 in maintaining liver homeostasis and tumor development, we created two liver-specific knockout mouse models with the deletion of Grp94 alone, or in combination with Pten, using the albumin-cre system. We demonstrated that while deletion of GRP94 in the liver led to hyperproliferation of liver progenitor cells, deletion of both GRP94 and PTEN accelerated development of liver tumors, including both hepatocellular carcinoma (HCC) and cholangiocarcinoma (CC), suggestive of progenitor cell origin. Furthermore, at the premalignant stage we observed disturbance of cell adhesion proteins and minor liver injury. When GRP94 was deleted in PTEN-null livers, ERK was selectively activated.
conclusionGRP94 is a novel regulator of cell adhesion, liver homeostasis, and tumorigenesis.
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