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. 2020 Aug;9(8):4906-4913.
doi: 10.21037/tcr-20-2246.

Glutaminase 2 functions as a tumor suppressor gene in gastric cancer

Liang Xu  1 , Dong Zhou  1 , Fang Li  1 , Lijiang Ji  1
Affiliations

Glutaminase 2 functions as a tumor suppressor gene in gastric cancer

Liang Xu et al. Transl Cancer Res. 2020 Aug.

Abstract

Background: Glutaminase 2 (GLS2) has been described as a tumor suppressor in hepatocellular carcinoma (HCC) and colon cancer. This study aimed to investigate the expression of GLS2 and its biological role in gastric cancer.

Methods: The expression of GLS2 was determined by quantitative Real-time PCR (qRT-PCR). Proliferation assay was performed by Cell Counting Kit-8 assay. Cell apoptosis assay was performed by Annexin V-fluorescein isothiocyanate (FITC) Apoptosis Detection Kit. Migration capability analysis was performed by Transwell chamber assay. The protein GLS2 and caspase 3 was determined by western blotting.

Results: Here, we demonstrated that GLS2 displayed a significant downregulation in gastric cancer tissues compared to adjacent non-cancer tissues, which suggested that the downregulation of GLS2 might possibly be associated with the development and progression of gastric cancer. We also found that GLS2 overexpression could significantly suppress gastric cancer cell proliferation and migration and enhance gastric cancer cell apoptosis via upregulating the expression of caspase 3.

Conclusions: These data taken together show that GLS2 functions as a tumor suppressor gene in gastric cancer. This study not only enriches the molecular mechanism of gastric cancer but also supplies a scientific basis for targeted treatment of gastric cancer.

Keywords: Glutaminase 2 (GLS2); gastric cancer; metastasis; proliferation.

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Conflict of interest statement

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at http://dx.doi.org/10.21037/tcr-20-2246). The authors have no conflicts of interest to declare.

Figures

Figure 1
Figure 1
GLS2 mRNA expression in gastric cancer tissues. **, P<0.01. GLS2, glutaminase 2.
Figure 2
Figure 2
GLS2 protein expression in gastric cancer cell lines from the non-transfected control group, the transfected empty vector control group, and the GLS2 overexpression vector-transfected group. **, P<0.01 compared to the non-transfected control group or the transfected empty vector control group. GLS2, glutaminase 2.
Figure 3
Figure 3
Effects of GLS2 on proliferation the ability of gastric cancer cells from the non-transfected control group, the transfected empty vector control group, and the GLS2 overexpression vector-transfected group. **, P<0.01 compared to the non-transfected control group or the transfected empty vector control group. GLS2, glutaminase 2.
Figure 4
Figure 4
Effects of GLS2 on apoptosis of gastric cancer cells from the non-transfected control group, the transfected empty vector control group and the GLS2 overexpression vector-transfected group. (A) Effects of GLS2 on gastric cancer cell apoptosis, (B) effects of GLS2 on caspase 3 in gastric cancer cells, (C) the relative expression of caspase three protein in gastric cancer cells. **, P<0.01 compared to the non-transfected control group or the transfected empty vector control group. GLS2, glutaminase 2.
Figure 5
Figure 5
Effects of GLS2 on migration ability of gastric cancer cells from the non-transfected control group, the transfected empty vector control group, and the GLS2 overexpression vector-transfected group. **, P<0.01 compared to the non-transfected control group or the transfected empty vector control group. GLS2, glutaminase 2.
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