ArticleMolecular and cellular biochemistry2017
Tubulin alpha 8 is expressed in hepatic stellate cells and is induced in transformed hepatocytes.
Article in Molecular and cellular biochemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
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- Systems biology approach to identify biomarkers and therapeutic targets for colorectal cancer.Biochemistry and biophysics reports · 2024Article
- Long-Term Phellodendri Cortex Supplementation in the Tiger Grouper (Life (Basel, Switzerland) · 2023Article
- Hepatocyte expressed chemerin-156 does not protect from experimental non-alcoholic steatohepatitis.Molecular and cellular biochemistry · 2022Article
- Dysregulation of SAA1, TUBA8 and Monocytes Are Key Factors in Ankylosing Spondylitis With Femoral Head Necrosis.Frontiers in immunology · 2021Article
- FAM172A affects cell proliferation and apoptosis not by targeting β-tubulin in HepG2 cells.Translational cancer research · 2020Article
- Gene Expression and DNA Methylation Alterations During Non-alcoholic Steatohepatitis-Associated Liver Carcinogenesis.Frontiers in genetics · 2019Article
- Alpha-syntrophin dependent expression of tubulin alpha 8 protein in hepatocytes.Journal of physiology and biochemistry · 2018Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tubulin alpha 8 (TUBA8) is highly abundant in murine liver tumors suggesting a role in hepatocellular carcinoma (HCC). Non-alcoholic steatohepatitis (NASH) is a risk factor for HCC. In mice that are fed with a methionine-choline deficient diet for two weeks to induce advanced murine NASH, we do see increased hepatic levels of TUBA8 protein. In animals given a high-fat diet for 14 weeks or an atherogenic diet for 12 weeks, hepatic TUBA8 is unchanged. TUBA8 is highly expressed in human hepatic stellate cells (HSC) and co-localizes with the HSC marker desmin in the murine liver. Inflammatory (TNF, LPS, IL-6) and profibrotic mediators (TGF-beta) do not regulate TUBA8 in HepG2 cells, primary HSC and the HSC cell line LX-2, when stimulated for 24 h. Agonists of the farnesoid X receptor and peroxisome proliferator activated receptor gamma, which are nuclear receptors involved in NASH and HCC pathophysiology, have no effect on TUBA8 in HepG2 and LX-2 cells. In human HCC tissues of 18 patients TUBA8 is significantly upregulated when compared to the corresponding non-tumorous tissues. Compared to non-transformed hepatocytes, TUBA8 protein is strongly expressed in transformed cells. Thus, TUBA8 is a marker of HSC whose cell number is increased in NASH, while higher levels in HCC may be related to induction of TUBA8 in parenchymal cells.
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