Reproductive and Developmental Biology

The Korean Society of Animal Reproduction (한국동물번식학회)
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Expression of C6orf62 in Human Embryonic Stem Cells and Cancer Cells

인간 배아 줄기세포와 암 세포에서의 C6orf62의 발현 패턴

  • Yoo, Han-Na (Dept. of Biomedical Science, College of Life Science, CHA University) ;
  • Yoo, Jung-Ki (Dept. of Biomedical Science, College of Life Science, CHA University) ;
  • Choi, Seoung-Jun (Dept. of Biomedical Science, College of Life Science, CHA University) ;
  • Kim, Jin-Kyeoung (Dept. of Biomedical Science, College of Life Science, CHA University)
  • 유한나 (차의과학대학교 의생명과학대학원 유전자조절실험실) ;
  • 류중기 (차의과학대학교 의생명과학대학원 유전자조절실험실) ;
  • 최성준 (차의과학대학교 의생명과학대학원 유전자조절실험실) ;
  • 김진경
  • Received : 2010.09.10
  • Accepted : 2010.09.17
  • Published : 2010.09.30
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Abstract

Pluripotency and self-renewal capacity of human embryonic stem cells (hESCs) are retained by hESCs related genes as OCT4, SOX2 and NANOG. These genes are shown high expression level in diverse cancer cells and have potential role in the carcinogenesis. On the contrary to this, several genes which are up-regulated in the differentiated hESCs are involved to suppress the carcinogenesis or proliferation of cells. We discovered several genes in immortalized lung fibroblast (WI-38 VA13) by suppression subtractive hybridization. Among them, we focused chromosome 6 open reading frame 62 (C6orf62) which is uncharacterized, mapped to 6p22.3 and generated to Hepatitis B virus X-transactivated proteins (HBVx-transactivated proteins, XTP). Aim of this study was to characterize C6orf62 through analyzing of expression pattern in various cell lines. Expression of C6orf62 was significantly upregulated in diverse normal cell lines than cancer cell lines. And C6orf62 was up-regulated in differentiated hESCs (endothelial cells, neural cells) compared to those of undifferentiated hESCs. Also, C6orf62 in WI-38 cells was highly up-regulated during G1/S transition of the cell cycle. Taken together, C6orf62 is shown expression pattern similar to differentiated hESCs-associated genes which down-regulated in cancer cells. Therefore, we assume that C6orf62 may participate to suppress the proliferation and to induce differentiation through regulating the cell cycle.

Keywords

References

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