GNG11 (G-protein subunit γ 11) suppresses cell growth with induction of reactive oxygen species and abnormal nuclear morphology in human SUSM-1 cells

Yuki Takauji, Ikuru Kudo, Atsuki En, Ryo Matsuo, Mohammad Nazir Hossain, Kazuhiko Nakabayashi, Kensuke Miki, Michihiko Fujii, Dai Ayusawa

Research output: Contribution to journalArticlepeer-review

17 Citations (Scopus)

Abstract

Enforced expression of GNG11, G-protein subunit γ 11, induces cellular senescence in normal human diploid fibroblasts. We here examined the effect of the expression of GNG11 on the growth of immortalized human cell lines, and found that it suppressed the growth of SUSM-1 cells, but not of HeLa cells. We then compared these two cell lines to understand the molecular basis for the action of GNG11. We found that expression of GNG11 induced the generation of reactive oxygen species (ROS) and abnormal nuclear morphology in SUSM-1 cells but not in HeLa cells. Increased ROS generation by GNG11 would likely be caused by the down-regulation of the antioxidant enzymes in SUSM-1 cells. We also found that SUSM-1 cells, even under normal culture conditions, showed higher levels of ROS and higher incidence of abnormal nuclear morphology than HeLa cells, and that abnormal nuclear morphology was relevant to the increased ROS generation in SUSM-1 cells. Thus, SUSM-1 and HeLa cells showed differences in the regulation of ROS and nuclear morphology, which might account for their different responses to the expression of GNG11. Thus, SUSM-1 cells may provide a unique system to study the regulatory relationship between ROS generation, nuclear morphology, and G-protein signaling.

Original languageEnglish
Pages (from-to)517-523
Number of pages7
JournalBiochemistry and Cell Biology
Volume95
Issue number4
DOIs
Publication statusPublished - 2017
Externally publishedYes

Keywords

  • Cellular immortalization
  • Cellular senescence
  • GNG11
  • Nuclear shape
  • Reactive oxygen species

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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