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Open Access Research article

Transdifferentiation-inducing HCCR-1 oncogene

Seon-Ah Ha1, Hyun K Kim1, JinAh Yoo1, SangHee Kim1, Seung M Shin1, Youn S Lee2, Soo Y Hur3, Yong W Kim3, Tae E Kim3, Yeun J Chung4, Shin S Jeun5, Dong W Kim6, Yong G Park7, Jin Kim8, Soon Y Shin9, Young H Lee9 and Jin W Kim13*

Author affiliations

1 Molecular Genetic Laboratory, Catholic Medical Research Institute, The Catholic University of Korea, Seoul, Korea

2 Department of Clinical Pathology, College of Medicine, The Catholic University of Korea, Seoul, Korea

3 Department of Obstetrics and Gynecology, College of Medicine, The Catholic University of Korea, Seoul, Korea

4 Department of Microbiology, College of Medicine, The Catholic University of Korea, Seoul, Korea

5 Department of Neurosurgery, College of Medicine, The Catholic University of Korea, Seoul, Korea

6 Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Korea

7 Department of Biostatistics, College of Medicine, The Catholic University of Korea, Seoul, Korea

8 Department of Anatomy, College of Medicine, The Catholic University of Korea, Seoul, Korea

9 Department of Biomedical Science and Technology, Research Center for Transcription Control, Institute of Biomedical Science and Technology, Konkuk University, Seoul, Korea

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Citation and License

BMC Cell Biology 2010, 11:49  doi:10.1186/1471-2121-11-49

Published: 30 June 2010

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.