Nat Commun: Multi-multi-dimensionalization of liver cells induces the occurrence of precancer lesions of hepatocellular carcinoma

Hepatocellular carcinoma (HCC) is the most important primary malignant tumor in the liver, accounting for 90% of all liver cancer cases, characterized by low survival rate.
genetic toxicity and related genetic model studies have shown that HCC cells originate from liver cells, and although there is growing evidence of the origin of HCC cells, it is not clear where the tumor lesions occur or why this transformation occurs.
studies have suggested that multiplying plays an important role in tumor occurrence.
most mammals are polyplos, but polyploupling occurs in specific organs, such as in the developing liver.
during postpartum development, liver cells develop into polyplocytes through incomplete cytospheric division formed by non-shrinking rings, which is also the main mechanism for the production of polyplate liver cells.
physiological hepatocellular multipliation is the diversity factor of liver stability, and also the relevant mechanism to limit cell proliferation and promote tumor inhibition.
the contribution of pathological polypolyxes caused by chronic stress or exposure to carcinogens to the development of cancer has yet to be studied.
In this study, ultra-polyhedr liver cells appeared in the CL and ML regions of the DEN-treated liver, and the researchers confirmed that the ultra-multiplication of liver cells around the small leaf (CL) region was closely related to the development of HCC cells after treatment with D.E. nitrosamine (DEN).
identified the advantages of the CL region for the accumulation of ultra-polyhedr liver cells and the formation of tumor folios in front of the tumor.
further studies have shown that the increase in the expression level of the Aurkb gene plays a key role in promoting ultra-multiplying of cells.
diagram of precancerous lesions produced by super-polyplurix liver cells detected an increase in phosphate levels of AURKB protein in intermediates during cytosusclic division, leading to the failure of cell division and the production of polyplification.
pharmacological inhibition of AORKB in the liver treated with methyl nitrosamines can significantly reduce the size of the nucleus and the number of tumor stoves around the CL region.
, the results reveal a close molecular link between hepatocellular pathological polyhedrations and HCC cell transformation in the CL region.