Degradation of plectin with modulation of cytokeratin 18 in human liver cells during staurosporine-induced apoptosis.

نویسندگان

  • Yi-Hsiang Liu
  • Chiung-Chi Cheng
  • Chin-Chin Ho
  • Wei-Ting Chao
  • Ren-Jeng Pei
  • Yung-Hsiang Hsu
  • Kun-Tu Yeh
  • Lu-Chang Ho
  • Ming-Chuang Tsai
  • Yih-Shyong Lai
چکیده

BACKGROUND Hepatoma cells are morphologically different from those of the normal liver. Intermediate filaments (IFs) are important in building the cellular architecture and maintaining the outline of cells. Plectin is a cross-linking protein that organizes the cytoskeleton into a stable meshwork, which can maintain the uniform size and shape of hepatocytes. Apoptosis might be the most possible pathway for creating plectin deficiency in the in vivo state. MATERIALS AND METHODS Apoptosis was induced by staurosporine (STS) treatment in liver cells. The protein expression of cytokeratin 18 (CK18) and plectin as well as the morphology of the liver cells and the distribution of CK18 and plectin in the cells was studied after STS treatment. RESULTS Plectin was cleaved in the liver cells during apoptosis and CK18 was modulated. Morphological changes were observed in the liver cells. CONCLUSION By affecting the organization of IFs, plectin might play an important role in the pleomorphism of hepatoma cells and even the tumorigenesis of hepatoma.

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عنوان ژورنال:
  • In vivo

دوره 22 5  شماره 

صفحات  -

تاریخ انتشار 2008