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Hyperpolyploidization of hepatocyte initiates preneoplastic lesion formation in the liver.

Abstract：

:Hepatocellular carcinoma (HCC) is the most predominant primary malignancy in the liver. Genotoxic and genetic models have revealed that HCC cells are derived from hepatocytes, but where the critical region for tumor foci emergence is and how this transformation occurs are still unclear. Here, hyperpolyploidization of hepatocytes around the centrilobular (CL) region is demonstrated to be closely linked with the development of HCC cells after diethylnitrosamine treatment. We identify the CL region as a dominant lobule for accumulation of hyperpolyploid hepatocytes and preneoplastic tumor foci formation. We also demonstrate that upregulation of Aurkb plays a critical role in promoting hyperpolyploidization. Increase of AURKB phosphorylation is detected on the midbody during cytokinesis, causing abscission failure and hyperpolyploidization. Pharmacological inhibition of AURKB dramatically reduces nucleus size and tumor foci number surrounding the CL region in diethylnitrosamine-treated liver. Our work reveals an intimate molecular link between pathological hyperpolyploidy of CL hepatocytes and transformation into HCC cells.

journal_name

Nat Commun

journal_title

Nature communications

authors

Lin H,Huang YS,Fustin JM,Doi M,Chen H,Lai HH,Lin SH,Lee YL,King PC,Hou HS,Chen HW,Young PY,Chao HW

doi

10.1038/s41467-020-20572-8

subject

Has Abstract

pub_date

2021-01-28 00:00:00

pages

645

issue

1

issn

2041-1723

pii

10.1038/s41467-020-20572-8

journal_volume

12

pub_type

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