Asset Details
Do you wish to reserve the book?
Hyperpolyploidization of hepatocyte initiates preneoplastic lesion formation in the liver
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Hyperpolyploidization of hepatocyte initiates preneoplastic lesion formation in the liver
Do you wish to request the book?
Hyperpolyploidization of hepatocyte initiates preneoplastic lesion formation in the liver
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Hyperpolyploidization of hepatocyte initiates preneoplastic lesion formation in the liver
2021
Overview
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.
Polyploidy is a common feature in normal hepatocytes, however, the pathophysiological function of hepatic hyperpolyploidy is unclear. Here, the authors show that genotoxic stress induces accumulation of hyperpolyploid hepatocytes around the centrilobular region of the liver, which may indicate the origin of preneoplastic formation.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 13/51
/ 14/19
/ 14/63
/ 38/39
/ 38/77
/ 38/90
/ 45/88
/ 49/31
/ 64/60
/ 82/80
/ Animals
/ Carcinoma, Hepatocellular - chemically induced
/ Carcinoma, Hepatocellular - genetics
/ Carcinoma, Hepatocellular - metabolism
/ Cell Transformation, Neoplastic - chemically induced
/ Cell Transformation, Neoplastic - genetics
/ Cell Transformation, Neoplastic - metabolism
/ Diethylnitrosamine - toxicity
/ Female
/ Humanities and Social Sciences
/ Humans
/ Lesions
/ Liver
/ Liver Neoplasms - chemically induced
/ Liver Neoplasms - metabolism
/ Male
/ Mice
/ Precancerous Conditions - chemically induced
/ Precancerous Conditions - genetics
/ Precancerous Conditions - metabolism
/ Science
/ Tumors
