Estrogen Receptor Beta Inhibits The Proliferation, Migration, And Angiogenesis Of Gastric Cancer Cells Through Inhibiting Nuclear Factor-Kappa B Signaling.
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ABSTRACT: Purpose:This study aimed to investigate the regulatory roles of estrogen receptor beta (ER?) on gastric cancer (GC) cells, and reveal the potential mechanisms relating to nuclear factor-kappa B (NF-?B) signaling. Methods:GC cell lines SGC7901 and MKN45 were transfected with pEGFP-C1-ER? to overexpress ER?, and treated with PMA (a NF-?B activator) to activate NF-?B signaling. The cell proliferation and migration, as well as the formation of vessel-like structures in human venous endothelial cells (HUVECs) were detected. The expression of ER?, NF-?B p65, p-NF-?B p65, Ki67 (a proliferation marker), vascular endothelial growth factor A (VEGF-A) and matrix metalloproteinase 2 (MMP-2), the DNA binding activity of NF-?B p65, the content of VEGF-A, and the activity of MMP-2 were detected in SGC7901 and MKN45 cells. Results:The transfection of pEGFP-C1-ER? significantly increased the expression of ER? in SGC7901 and MKN45 cells (P < 0.05). Overexpression of ER? in SGC7901 and MKN45 cells significantly decreased the cell activity, cell number in G2/M phase, cell migration, the expression of Ki67, VEGF-A and MMP-2, VEGF-A content, MMP-2 activity, as well as the number of vessel-like structures formed by HUVECs (P < 0.05). Overexpression of ER? also significantly decreased the DNA binding activity and the expression of p-NF-?B p65 in SGC7901 and MKN45 cells (P < 0.05). The anti-tumor effect of ER? overexpression on GC cells was reversed by the intervention of PMA (P < 0.05). Conclusion:Overexpression of ER? inhibited the proliferation, migration, and angiogenesis of GC cells through inhibiting NF-?B signaling.
SUBMITTER: Zhang Y
PROVIDER: S-EPMC6842292 | biostudies-literature | 2019
REPOSITORIES: biostudies-literature
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