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| http://dx.doi.org/10.1016/j.jcmgh.2023.10.010 | DOI Listing |
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NCOA5 Deficiency in Macrophages Provokes NASH and HCC.
Cell Mol Gastroenterol Hepatol
December 2023
Department of Pathology, School of Medicine, Department of Molecular Biology, School of Biological Sciences, University of California at San Diego, La Jolla, California. Electronic address:
NCOA5 Haploinsufficiency in Myeloid-Lineage Cells Sufficiently Causes Nonalcoholic Steatohepatitis and Hepatocellular Carcinoma.
Cell Mol Gastroenterol Hepatol
December 2023
Department of Physiology, Michigan State University, East Lansing, Michigan. Electronic address:
Background & Aims: The nuclear receptor coactivator 5 (NCOA5) is a putative type 2 diabetes susceptibility gene. NCOA5 haploinsufficiency results in the spontaneous development of nonalcoholic fatty liver disease (NAFLD), insulin resistance, and hepatocellular carcinoma (HCC) in male mice; however, the cell-specific effect of NCOA5 haploinsufficiency in various types of cells, including macrophages, on the development of NAFLD and HCC remains unknown.
Methods: Control and myeloid-lineage-specific Ncoa5 deletion (Ncoa5) mice fed a normal diet were examined for the development of NAFLD, nonalcoholic steatohepatitis (NASH), and HCC.
NCOA5 deficiency promotes a unique liver protumorigenic microenvironment through p21 overexpression, which is reversed by metformin.
Oncogene
May 2020
Department of Physiology, Michigan State University, East Lansing, Michigan, 48824, USA.
Prevention and treatment options for hepatocellular carcinoma (HCC) are presently limited, underscoring the necessity for further elucidating molecular mechanisms underlying HCC development and identifying new prevention and therapeutic targets. Here, we demonstrate a unique protumorigenic niche in the livers of Ncoa5 mouse model of HCC, which is characterized by altered expression of a subset of genes including p21 and proinflammatory cytokine genes, increased putative hepatic progenitors, and expansions of activated and tissue-resident memory (TRM) CD8+ T lymphocytes, myeloid-derived suppressor cells (MDSCs), and alternatively activated M2 macrophages. Importantly, prophylactic metformin treatment reversed these characteristics including aberrant p21 expression and subsequently reduced HCC incidence in Ncoa5 male mice.
View Article and Find Full Text PDFNCOA5 Haplo-insufficiency Results in Male Mouse Infertility through Increased IL-6 Expression in the Epididymis.
Sci Rep
October 2019
Department of Physiology, Michigan State University, East Lansing, Michigan, 48824, USA.
Male infertility might be caused by genetic and/or environmental factors that impair spermatogenesis and epididymal sperm maturation. Here we report that heterozygous deletion of the nuclear receptor coactivator-5 (Ncoa5) gene resulted in decreased motility and progression of spermatozoa in the cauda epididymis, leading to infertility in male mice. Light microscopic and ultrastructural analysis revealed morphological defects in the spermatozoa collected from the cauda epididymis of Ncoa5 mice.
View Article and Find Full Text PDFNCOA5 haploinsufficiency results in glucose intolerance and subsequent hepatocellular carcinoma.
Cancer Cell
December 2013
Department of Physiology, Michigan State University, East Lansing, MI 48824, USA. Electronic address:
Type 2 diabetes (T2D) and male gender are associated with hepatocellular carcinoma (HCC) development. We demonstrate that heterozygous deletion of the Ncoa5 gene causes spontaneous development of HCC exclusively in male mice. Tumor development is preceded by increased interleukin-6 (IL-6) expression, early-onset glucose intolerance, and progressive steatosis and dysplasia in livers.
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