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.
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http://dx.doi.org/10.1139/bcb-2016-0248 | DOI Listing |
FEBS J
May 2024
Graduate School of Nanobioscience, Yokohama City University, Japan.
Mammalian somatic cells undergo terminal proliferation arrest after a limited number of cell divisions, a phenomenon termed cellular senescence. However, cells acquire the ability to proliferate infinitely (cellular immortalization) through multiple genetic alterations. Inactivation of tumor suppressor genes such as p53, RB and p16 is important for cellular immortalization, although additional molecular alterations are required for cellular immortalization to occur.
View Article and Find Full Text PDFBiochem Cell Biol
August 2017
a Graduate School of Nanobioscience, Yokohama City University, 22-2 Seto, Kanazawa-ku, Yokohama, Kanagawa 236-0027, Japan.
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.
View Article and Find Full Text PDFJ Cataract Refract Surg
May 2006
Department of Ophthalmology, Tokyo Medical University Hospital, Tokyo, Japan.
Purpose: To investigate cell adhesion to intraocular lens (IOL) surfaces having different properties using bacteria and fibroblasts.
Setting: Department of Ophthalmology, Tokyo Medical University Hospital, Tokyo, Japan.
Methods: The polished acrylic IOLs VA60-BB and VA-60-CB (Hoya) were used with no coating or after coating with poly(2-methacryloyloxyethyl phosphocholine-co-n-butyl-methacrylate) (MPC) or methane gas plasma.
Exp Cell Res
April 2005
Kihara Institute for Biological Research and Graduate School of Integrated Science, Yokohama City University, Maioka-cho 641-12, Yokohama 244-0813, Japan.
We identified genes that immediately respond to 5-bromodeoxyuridine (BrdU) in SUSM-1, an immortal fibroblastic line, with DNA microarray and Northern blot analysis. At least 29 genes were found to alter gene expression greater than twice more or less than controls within 36 h after addition of BrdU. They took several different expression patterns upon addition of BrdU, and the majority showed a significant alteration within 12 h.
View Article and Find Full Text PDFCancer Cell Int
October 2002
Tokyo Women's Medical University, Kidney Center, Department of Surgery 8-1 Kawada-cho, Shinjuku-ku, Tokyo 162-8666, Japan.
BACKGROUND: We previously reported the usefulness of the alphaGal epitope as a target molecule for gene therapy against cancer. To induce cancer cell specific transcription of the alphaGal epitope, an expression vector which synthesizes the alphaGal epitope under the control of a promoter region of the human telomerase reverse transcriptase (hTERT), NK7, was constructed. METHODS: NK7 was transfected into a human pancreatic carcinoma cell line, MIA cells, and telomerase-negative SUSM-1 cells served controls.
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