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Archive > Volume 23 Issue 2 > 2016,23(2):250-254. DOI:10.3872/j.issn.1007-385X.2016.02.016 Prev Next
Basic Research
Role of ERK transduction signaling pathway in proliferation and invasion of endometrial carcinoma cells promoted by CXCL12
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Abstract:
Objective:To explore the role of chemokine CXCL12 and its receptor CXCR4 (biologic axis CXCL12/CXCR4) in promoting proliferation and invasion of endometrial carcinoma cells through transduction signaling pathway of extracellular signal-regulated kinase (ERK). Methods:Ishikawa endometrial carcinoma cell line was treated with exogenous CXCL12. The phosphorylation of ERK1/2 and the expression of survivin protein at different time points were detected by Western blotting; and secretion level of MMP-2 in supernatant of cell culture was measured by ELISA. At the same time, effects of AMD3100 and PD98059 on phosphorylation level of ERK1/2, level of Survivin protein and secretion level of MMP-2 were analyzed. Results: After treatment with exogenous CXCL12, phosphorylation level of ERK1/2 was rapidly risen (t=0.887，P<0.01）as well as expressions of Survivin and MMP-2 proteins were boosted(t=0.861，P<0.01; t=0.297，P<0.01) in a time dependent manner. Both of PD98059 and AMD3100 could significantly inhibit the phosphorylation level of p-ERK after induction with exogenous CXCL12. Combined action of PD98059 and AMD3100 could completely inhibit phosphorylation of ERK, block the activation of ERK pathway, and down-regulate the expressions of Survivin and MMP-2 proteins. Conclusion: Biologic axis of CXCL12/CXCR4 could up-regulate the expressions of Survivin and MMP-2 proteins through activation of ERK pathway, 〖JP3〗thus inspire a series of biological effects in proliferation and invasion of the Ishikawa cell.
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Project Supported:
Project supported by the Scientific Research Foundation of Shandong Province for Outstanding Young Scientist Award(No.BS2009SW002)，and the Natural Science Foundation of Shandong Province （No.ZR2013HM012）
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