Original article

Effects of CXCR2 on invasion, migration and apoptosis of gastric cancer cells

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  • 1. Department of General Surgery, Zhongshan Hospital (Qingpu Branch), Fudan University, Shanghai 201700, China
    2. Department of General Surgery, Zhongshan Hospital, Fudan University, Shanghai 200032, China

Received date: 2020-05-18

  Online published: 2022-07-22

Abstract

Objective To investigate the effects of C-X-C motif chemokine receptor 2 (CXCR2) on invasion, migration and apoptosis of gastric cancer cells. Methods Gastric cancer cells MGC80-3 and SGC-7901 with upregulated CXCR2 were established by stable Lentivirus transfection. CXCR2 gene silencing cells were established by plasmid transient transfection and RNA interference. Proteins related to cell phenotype changes were detected by Western blotting. The functional changes of cells were detected by transwell invasion and migration assays. Cell proliferation was measured by CCK8 assays. Apoptosis was detected by Annexin V-PI double staining of flow cytometry. CXCR2 mRNA was detected via real-time quantitative PCR. Results Upregulation of CXCR2 in gastric cancer cells exhibited an increased ability of cells migration and invasion (P<0.05) and reduced the apoptosis rate (P<0.01). Downregulation of CXCR2 inhibited the invasion and migration ability of gastric cancer cells(P<0.05) and increased the apoptosis rate(P=0.02). Phosphorylation level of Akt in gastric cancer cells which overexpressed CXCR2 was significantly upregulated. Phosphorylation level of Akt was consistent with the expression of apoptosis inhibitor protein Bcl-2. Conclusions Upregulation of CXCR2 enhanced the ability of invasion, migration and evasion of apoptosis of gastric cancer cell. The evasion of apoptosis was associated with CXCR2/Aki/Bcl-2 pathway.

Cite this article

LU Weihui, LIU Wei, WANG Cong, WANG Zhenglin . Effects of CXCR2 on invasion, migration and apoptosis of gastric cancer cells[J]. Journal of Surgery Concepts & Practice, 2021 , 26(05) : 430 -436 . DOI: 10.16139/j.1007-9610.2021.05.014

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