Open AccessProlonged silencing of diacylglycerol acyltransferase‐1 induces a dedifferentiated phenotype in human liver cells
Author(s) -
Chang Soyoung,
Sung Pil Soo,
Lee Jungsul,
Park Junseong,
Shin EuiCheol,
Choi Chulhee
Publication year - 2016
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.12685
Subject(s) - diacylglycerol kinase , gene silencing , steatosis , microbiology and biotechnology , biology , medicine , endocrinology , gene , biochemistry , signal transduction , protein kinase c
Diacylglycerol acyltransferase‐1 ( DGAT 1), a key enzyme in triglyceride ( TG ) biogenesis, is highly associated with metabolic abnormalities, such as obesity and type 2 diabetes. However, the effects of DGAT 1 silencing in the human liver have not been elucidated. To investigate the effects of DGAT 1 silencing in human liver cells, we compared the cellular behaviours of DGAT 1‐deficient Huh‐7.5 cell lines with those of control Huh‐7.5 cells. DGAT 1‐deficient cells acquired dedifferentiated and stem cell‐like characteristics, such as formation of aggregates in the presence of high levels of growth factors, high proliferation rates and loss of albumin secretion. In relation to aggregate formation, the expression level of various adhesion molecules was significantly altered in DGAT 1‐deficient cells. Microarray data analysis and immunostaining of patient tissue samples clearly showed decreased expression levels of DGAT 1 and integrin β1 in patients who have nodular cirrhosis without fatty degeneration.