Liver-specific deletion of miR-181ab1 reduces liver tumour progression via upregulation of CBX7 View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2022-07-22

AUTHORS

Jinbiao Chen, Yang Zhao, Fan Zhang, Jia Li, Jade A. Boland, Ngan Ching Cheng, Ken Liu, Jessamy C. Tiffen, Patrick Bertolino, David G. Bowen, Andreas Krueger, Leszek Lisowski, Ian E. Alexander, Mathew A. Vadas, Emad El-Omar, Jennifer R. Gamble, Geoffrey W. McCaughan

ABSTRACT

MiR-181 expression levels increased in hepatocellular carcinoma (HCC) compared to non-cancerous tissues. MiR-181 has been widely reported as a possible driver of tumourigenesis but also acts as a tumour suppressor. In addition, the miR-181 family regulates the development and function of immune and vascular cells, which play vital roles in the progression of tumours. More complicatedly, many genes have been identified as miR-181 targets to mediate the effects of miR-181. However, the role of miR-181 in the development of primary tumours remains largely unexplored. We aimed to examine the function of miR-181 and its vital mediators in the progression of diethylnitrosamine-induced primary liver cancers in mice. The size of liver tumours was significantly reduced by 90% in global (GKO) or liver-specific (LKO) 181ab1 knockout mice but not in hematopoietic and endothelial lineage-specific knockout mice, compared to WT mice. In addition, the number of tumours was significantly reduced by 50% in GKO mice. Whole-genome RNA-seq analysis and immunohistochemistry showed that epithelial-mesenchymal transition was partially reversed in GKO tumours compared to WT tumours. The expression of CBX7, a confirmed miR-181 target, was up-regulated in GKO compared to WT tumours. Stable CBX7 expression was achieved with an AAV/Transposase Hybrid-Vector System and up-regulated CBX7 expression inhibited liver tumour progression in WT mice. Hepatic CBX7 deletion restored the progression of LKO liver tumours. MiR-181a expression was the lowest and CBX7 expression the highest in iClust2 and 3 subclasses of human HCC compared to iClust1. Gene expression profiles of GKO tumours overlapped with low-proliferative peri-portal-type HCCs. Liver-specific loss of miR-181ab1 inhibited primary liver tumour progression via up-regulating CBX7 expression, but tumour induction requires both hepatic and non-hepatic miR-181. Also, miR-181ab1-deficient liver tumours may resemble low-proliferative periportal-type human HCC.Graphical abstractmiR-181 was increased with liver tumour growth. More miR-181, darker colour and higher shape. CBX7 was very low in pericentral hepatocytes, increased in early liver tumours, but reduced in advanced liver tumours. Its levels were maintained in miR-181 KO liver tumours. In tumours (T), brown (darker is more) represents miR-181, the blue circle (thicker is more) represents CBX7. More... »

PAGES

443

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  • Journal

    TITLE

    Cellular and Molecular Life Sciences

    ISSUE

    8

    VOLUME

    79

    Author Affiliations

  • Liver Injury and Cancer Program Centenary Institute and Sydney Medical School, Faculty of Medicine and Health, The University of Sydney, 2050, Camperdown, NSW, Australia
  • School of Medicine and Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing, People’s Republic of China
  • UNSW Microbiome Research Centre, School of Clinical Medicine, UNSW Medicine and Health, St George and Sutherland Clinical Campuses, 2217, Kogarah, NSW, Australia
  • Centre for Motor Neuron Disease, Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Macquarie University, 2109, Sydney, NSW, Australia
  • Vascular Biology Program Centenary Institute and Sydney Medical School, Faculty of Medicine and Health, The University of Sydney, 2050, Camperdown, NSW, Australia
  • Royal Prince Alfred Hospital, Missenden Road, 2050, Camperdown, NSW, Australia
  • Melanoma Epigenetics Lab Centenary Institute and Sydney Medical School, Faculty of Medicine and Health, The University of Sydney, 2050, Camperdown, NSW, Australia
  • Liver Immunology Program Centenary Institute and Sydney Medical School, Faculty of Medicine and Health, The University of Sydney, 2050, Camperdown, NSW, Australia
  • Institute for Molecular Medicine, Frankfurt Cancer Institute, Goethe-University, Frankfurt, Germany
  • Laboratory of Molecular Oncology and Innovative Therapies, Military Institute of Medicine, Warsaw, Poland
  • Gene Therapy Research Unit, Children’s Medical Research Institute, Faculty of Medicine and Health, The University of Sydney and Sydney Children’s Hospitals Network, 2145, Westmead, NSW, Australia
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1007/s00018-022-04452-6

    DOI

    http://dx.doi.org/10.1007/s00018-022-04452-6

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1149686684

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/35867177


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