Overexpression of SIRT4 inhibits the proliferation of gastric cancer cells through cell cycle arrest

The sirtuins (SIRTs) are a family of nicotinamide-adenine dinucleotide (NAD) -dependent protein deacetylases. SIRT4 is a mitochondrial NAD -dependent adenosine diphsophate-ribosyltransferase. Recent studies demonstrated that SIRT4 can regulate glutamine metabolism and thus act as a tumor suppressor....

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Bibliographic Details
Published in:Oncology letters 2019-02, Vol.17 (2), p.2171-2176
Main Authors: Hu, Yiwang, Lin, Jiahao, Lin, Yao, Chen, Xuxu, Zhu, Guanbao, Huang, Guoyu
Format: Article
Language:English
Subjects:
Biotechnology
Cancer
Cancer cells
Care and treatment
Cell cycle
Cell growth
Development and progression
Esophageal cancer
Flow cytometry
Gastric cancer
Gene expression
Genetic aspects
Glutamine
Health aspects
Infection
Kinases
Lymphoma
Metabolism
Niacinamide
Pathogenesis
Phase transitions
Polyclonal antibodies
Prostate cancer
Proteins
Purines
Signaling peptides and proteins
Stomach cancer
Studies
Tumors
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Summary:The sirtuins (SIRTs) are a family of nicotinamide-adenine dinucleotide (NAD) -dependent protein deacetylases. SIRT4 is a mitochondrial NAD -dependent adenosine diphsophate-ribosyltransferase. Recent studies demonstrated that SIRT4 can regulate glutamine metabolism and thus act as a tumor suppressor. However, the association of SIRT4 with gastric cancer remains unknown. The present study investigated the potential role of SIRT4 in the proliferation of human gastric cancer cells. Gastric cancer cell lines (SGC-7901 and MNK45) overexpressing SIRT4 were established by lentiviral infection. The effect of overexpression of SIRT4 in gastric cancer was evaluated by determining the cell viability, proliferation activity and colony-forming ability of gastric cancer cells . Furthermore, the cell cycle profiles of SGC-7901 and MNK45 cells overexpressing SIRT4 were evaluated to provide insights into potential underlying molecular mechanisms. Overexpression of SIRT4 significantly inhibited the proliferation and colony-forming ability of the gastric cancer cells . Furthermore, overexpression of SIRT4 induced G1 cell cycle arrest via suppression of phosphorylated extracellular signal-regulated kinase, cyclin D and cyclin E. In conclusion, the results of the present study indicated that SIRT4 may function as a tumor suppressor in gastric cancer by regulating cell proliferation, therefore SIRT4 may be a potential therapeutic target against this disease.
ISSN:1792-1074
1792-1082
DOI:10.3892/ol.2018.9877