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P42 Ebp1 functions as a tumor suppressor in non-small cell lung cancer

  • Ko, Hyo Rim (Department of Molecular Cell Biology, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine) ;
  • Nguyen, Truong L.X. (Department of Molecular Cell Biology, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine) ;
  • Kim, Chung Kwon (Department of Molecular Cell Biology, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine) ;
  • Park, Youngbin (Department of Biology, Johns Hopkins University) ;
  • Lee, Kyung-Hoon (Anatomy, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine) ;
  • Ahn, Jee-Yin (Department of Molecular Cell Biology, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine)
  • 투고 : 2014.06.17
  • 심사 : 2014.07.02
  • 발행 : 2015.03.31

초록

Although the short isoform of ErbB3-binding protein 1 (Ebp1), p42 has been considered to be a potent tumor suppressor in a number of human cancers, whether p42 suppresses tumorigenesis of lung cancer cells has never been clarified. In the current study we investigated the tumor suppressor role of p42 in non-small cell lung cancer cells. Our data suggest that the expression level of p42 is inversely correlated with the cancerous properties of NSCLC cells and that ectopic expression of p42 is sufficient to inhibit cell proliferation, anchorage-independent growth, and invasion as well as tumor growth in vivo. Interestingly, p42 suppresses Akt activation and overexpression of a constitutively active form of Akt restores the tumorigenic activity of A549 cells that is ablated by exogenous p42 expression. Thus, we propose that p42 Ebp1 functions as a potent tumor suppressor of NSCLC through interruption of Akt signaling.

키워드

참고문헌

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