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Cytoglobin inhibits migration through PI3K/AKT/mTOR pathway in fibroblast cells.

  1. Author:
    Demirci, Selami
    Dogan, Aysegul
    Apdik, Hüseyin
    Tuysuz, Emre Can
    Gulluoglu, Sukru
    Bayrak, Omer Faruk
    Sahin, Fikrettin
  2. Author Address

    Department of Genetics and Bioengineering, Faculty of Engineering and Architecture, Yeditepe University, Kayisdagi Cad. 26 Agustos Yerlesimi, 34755, Atasehir, Istanbul, Turkey., National Heart, Lung, and Blood Institute (NHLBI), NIH, Bethesda, MD, USA., Department of Genetics and Bioengineering, Faculty of Engineering and Architecture, Yeditepe University, Kayisdagi Cad. 26 Agustos Yerlesimi, 34755, Atasehir, Istanbul, Turkey. aysegul.dogan@nih.gov., National Cancer Institute, CDBL, NIH, Frederick, MD, USA. aysegul.dogan@nih.gov., Department of Medical Genetics, Yeditepe University Medical School Inonu Mah, Kayisdagi Cad. 26 Agustos Yerlesimi, 34755, Atasehir, Istanbul, Turkey.,
    1. Year: 2018
    2. Date: Jan
    3. Epub Date: 2017 Jun 15
  1. Journal: Molecular and cellular biochemistry
    1. 437
    2. 1-2
    3. Pages: 133-142
  2. Type of Article: Article
  3. ISSN: 0300-8177
  1. Abstract:

    Cell proliferation and migration are crucial in many physiological processes including development, cancer, tissue repair, and wound healing. Cell migration is regulated by several signaling molecules. Identification of genes related to cell migration is required to understand molecular mechanism of non-healing chronic wounds which is a major concern in clinics. In the current study, the role of cytoglobin (CYGB) gene in fibroblast cell migration and proliferation was described. L929 mouse fibroblast cells were transduced with lentiviral particles for CYGB and GFP, and analyzed for cell proliferation and migration ability. Fibroblast cells overexpressing CYGB displayed decreased cell proliferation, colony formation capacity, and cell migration. Phosphorylation levels of mTOR and two downstream effectors S6 and 4E-BP1 which take part in PI3K/AKT/mTOR signaling declined in CYGB-overexpressing cells. Microarray analysis indicated that CYGB overexpression leads to downregulation of cell proliferation, migration, and tumor growth associated genes in L929 cell line. This study demonstrated the role of CYGB in fibroblast cell motility and proliferation. CYGB could be a promising candidate for further studies as a potential target for diseases related to cell migration such as cancer and chronic wound treatment.

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External Sources

  1. DOI: 10.1007/s11010-017-3101-2
  2. PMID: 28620820
  3. WOS: 000419379100011

Library Notes

  1. Fiscal Year: FY2016-2017
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