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PKMYT1 promoted the growth and motility of hepatocellular carcinoma cells by activating beta-catenin/TCF signaling

Exp Cell Res. 2017 Sep 15;358(2):209-216. doi: 10.1016/j.yexcr.2017.06.014. Epub 2017 Jun 23.

Abstract

Over-activation of beta-catenin/TCF signaling has been frequently observed in hepatocellular carcinoma (HCC). Better understanding the molecular mechanism for the aberrant activation of beta-catenin/TCF signaling would provide novel insights into the treatment of this malignancy. In this study, we have shown that the expression of PKMYT1 was up-regulated in HCC. PKMYT1 positively regulated the growth, migration, colony formation, metastasis and epithelia mesenchymal transition (EMT) of HCC cells. Mechanically, PKMTY1 activated the beta-catenin/TCF signaling by binding and inactivating GSK3beta. Taken together, our study demonstrated the oncogenic activity of PKMYT1 in the progression of HCC and suggested that PKMYT1 might be a therapeutic target.

Keywords: Beta-catenin/TCF; Epithelial mesenchymal transition; Hepatocellular carcinoma; PKMYT1.

MeSH terms

  • Carcinoma, Hepatocellular / metabolism*
  • Cell Line, Tumor
  • Cell Movement / physiology
  • Epithelial-Mesenchymal Transition / physiology
  • Gene Expression Regulation, Neoplastic / genetics*
  • Humans
  • Liver Neoplasms / metabolism*
  • Liver Neoplasms / pathology
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism*
  • Protein Serine-Threonine Kinases / genetics
  • Protein Serine-Threonine Kinases / metabolism*
  • Protein-Tyrosine Kinases / genetics
  • Protein-Tyrosine Kinases / metabolism*
  • Signal Transduction* / physiology
  • TCF Transcription Factors / metabolism
  • beta Catenin / metabolism

Substances

  • CTNNB1 protein, human
  • Membrane Proteins
  • TCF Transcription Factors
  • beta Catenin
  • Protein-Tyrosine Kinases
  • PKMYT1 protein, human
  • Protein Serine-Threonine Kinases