Abstract

Previous studies have reported an important role of c-kit in embryogenesis and adulthood. Activation of the SCF/KIT signal transduction pathway is customarily linked to cell proliferation, migration and survival thus influence hematopoiesis, pigmentation, and spermatogenesis. The role of c-kit in the liver is controversial, it is however argued that it is a double-edged sword in liver regeneration and diseases. First, liver c-kit+ cells, including oval cells, bile epithelial cells, and part of hepatocytes, participate in liver tissue repair by regenerating target cells according to the type of liver injury. At the same time, c-kit+ mast cells, act as immature progenitors in circulation, playing a critical role in liver fibrosis. Furthermore, c-kit is also a proto-oncogene. Notably, c-kit overexpression regulates gastrointestinal stromal tumors. Various studies have explored on c-kit and hepatocellular carcinoma, nevertheless, the intricate roles of c-kit in the liver are largely understudied. Herein, we extensively summarize previous studies geared toward providing hints for future clinical and basic research.

Highlights

  • C-kit known as CD117, is a type III receptor tyrosine kinase coded by the KIT gene

  • C-kit can be used as an early diagnostic factor for HBV-related HCC

  • C-kit+ mast cells increase after liver allograft rejection, but the increased c-kit+ mast cells cannot distinguish rejection from recurrent HCV infection in transplantation of liver

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Summary

Introduction

C-kit known as CD117, is a type III receptor tyrosine kinase coded by the KIT gene. The role of c-kit in the liver is conflicting, it is a two-edged sword in liver regeneration and diseases. As a liver stem cell marker, c-kit+ cells, such as oval cells, BECs, and part of C-kit can be used as an early diagnostic factor for HBV-related HCC.

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