ArticleJournal of gastroenterology and hepatology2013
Association of cyclin D and estrogen receptor α36 with hepatocellular adenomas of female mice under chronic endoplasmic reticulum stress.
Article in Journal of gastroenterology and hepatology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Sappanchalcone suppresses NSCLC by oxidative stress-driven DNA damage and ER stress activation through PIEZO1 modulation.iScience · 2025Article
- Estrobolome and Hepatocellular Adenomas-Connecting the Dots of the Gut Microbial β-Glucuronidase Pathway as a Metabolic Link.International journal of molecular sciences · 2023Review
- Estrogen receptor-α36-mediated rapid estrogen signaling regulates 78 kDa glucose-regulated protein expression in gastric carcinoma cells.Oncology letters · 2018Article
- Advances and New Concepts in Alcohol-Induced Organelle Stress, Unfolded Protein Responses and Organ Damage.Biomolecules · 2015Review
- The potential for chemical mixtures from the environment to enable the cancer hallmark of sustained proliferative signalling.Carcinogenesis · 2015Review
- Stat3 is a candidate epigenetic biomarker of perinatal Bisphenol A exposure associated with murine hepatic tumors with implications for human health.Epigenetics · 2015Article
- New Insights into the Pathogenesis of Alcohol-Induced ER Stress and Liver Diseases.International journal of hepatology · 2014Review
- Altered methylation and expression of ER-associated degradation factors in long-term alcohol and constitutive ER stress-induced murine hepatic tumors.Frontiers in genetics · 2013Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
BACKGROUND AND
aimsHepatocellular adenomas (HCAs) are benign tumors that can lead to medical complications. Chronic inflammation and mutations in β-catenin, hepatocyte nuclear factor 1α, or glycoprotein 130 are potential causes for human HCA. However, additional causes may exist due to heterogeneity of HCA. We investigated whether HCA are caused by endoplasmic reticulum (ER) stress.
methodsMice with a liver-specific deletion of the major chaperone BiP (LGKO) were used. Liver tumor occurrence was examined in LGKO with or without feeding of a high-fat diet (HFD) and characterized with immunohistochemistry with molecular markers of proliferation/malignancy. Molecular changes were analyzed with immunoblotting.
resultsSpontaneous monoclonal liver tumors were observed in 34% of LGKO females with constitutive hepatic ER stress. Lack of portal tracks or central veins, dilated sinusoidal spaces, hemorrhagic areas, active proliferation, and lipid deposits were observed in the liver tumors. HFD feeding induced multiclonal liver tumors in 83% of the LGKO females versus 0 in wild-type females. Hepatocytes reactive to antiglypican 3 antibodies were detected in the HFD-induced, but not spontaneous, tumors. In the liver tumors, inhibition of cyclin D and increase of the 36 kD estrogen receptor variant (estrogen receptor α36), active transcription activator 4/6, glycogen synthase kinase 3β, and extracellular signal-regulated protein kinases 1 and 2 were detected, whereas no change of hepatocyte nuclear factor 1α, β-catenin, p-53, androgen receptor α, or estrogen receptor α was detected. HFD activated Janus kinase and signal transducers and activators of transcription 3.
conclusionsOur evidence supports a novel link of HCA with ER stress and altered expression of cyclin D and estrogen receptor α36. Additional stress such as HFD may promote malignant transformation of HCA through the Janus kinase-signal transducers and activators of transcription pathway.
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