Transdifferentiation-inducing HCCR-1 oncogene

BMC Cell Biol. 2010 Jun 30:11:49. doi: 10.1186/1471-2121-11-49.

Abstract

Background: Cell transdifferentiation is characterized by loss of some phenotypes along with acquisition of new phenotypes in differentiated cells. The differentiated state of a given cell is not irreversible. It depends on the up- and downregulation exerted by specific molecules.

Results: We report here that HCCR-1, previously shown to play an oncogenic role in human cancers, induces epithelial-to-mesenchymal transition (EMT) and mesenchymal-to-epithelial transition (MET) in human and mouse, respectively. The stem cell factor receptor CD117/c-Kit was induced in this transdifferentiated (EMT) sarcoma tissues. This MET occurring in HCCR-1 transfected cells is reminiscent of the transdifferentiation process during nephrogenesis. Indeed, expression of HCCR-1 was observed during the embryonic development of the kidney. This suggests that HCCR-1 might be involved in the transdifferentiation process of cancer stem cell.

Conclusions: Therefore, we propose that HCCR-1 may be a regulatory factor that stimulates morphogenesis of epithelia or mesenchyme during neoplastic transformation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Transdifferentiation*
  • Cell Transformation, Neoplastic*
  • Cloning, Molecular
  • Gene Expression Regulation, Developmental
  • Humans
  • Kidney / embryology
  • Kidney / metabolism*
  • Kidney / pathology
  • Mice
  • Mice, Inbred BALB C
  • Mice, Nude
  • NIH 3T3 Cells
  • Neoplasm Transplantation
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins / metabolism*
  • Proto-Oncogene Proteins c-kit / biosynthesis*
  • Proto-Oncogene Proteins c-kit / genetics
  • Transgenes / genetics

Substances

  • LETMD1 protein, human
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-kit