Involvement of ephrin receptor A4 in pancreatic cancer cell motility and invasion | Zendy

Chengli Liu | Zendy; Hui Huang | Zendy; Cheng Wang | Zendy; Yalin Kong | Zendy; Hongyi Zhang | Zendy

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Involvement of ephrin receptor A4 in pancreatic cancer cell motility and invasion

Author(s) -

Chengli Liu,

Hui Huang,

Cheng Wang,

Yalin Kong,

Hongyi Zhang

Publication year - 2014

Publication title -

oncology letters

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.766

H-Index - 54

eISSN - 1792-1082

pISSN - 1792-1074

DOI - 10.3892/ol.2014.2011

Subject(s) - pancreatic cancer , erythropoietin producing hepatocellular (eph) receptor , gene knockdown , ephrin , downregulation and upregulation , motility , cancer research , biology , eph receptor a2 , small interfering rna , cancer cell , tumor progression , receptor , cancer , microbiology and biotechnology , transfection , cell culture , signal transduction , receptor tyrosine kinase , biochemistry , genetics , gene

Ephrin (EPH) receptors can be classified into EPHA and EPHB receptors and are important in diverse cellular processes. EPHA4, a member of the EPHA receptors, has been demonstrated to be elevated in various human cancers and involved in the tumor progression. However, the role of EPHA4 in pancreatic cancer cells remains unclear. Therefore, the present study transfected Panc-1 and BxPC-3 cells with small interfering RNA (siRNA) to knockdown the expression of EPHA4. Wound healing and invasion assays were then performed to assess the effect of EPHA4 knockdown on the motility and invasion of pancreatic cancer cells. The results demonstrated that the knockdown of EPHA4 by siRNA inhibits the motility and invasion of pancreatic cancer cells. Furthermore, gelatin zymography assay showed that EPHA4 may regulate the activity of matrix metalloproteinase (MMP)-2. In addition, the knockdown of EPHA4 increased the expression of epithelial (E)-cadherin, as well as decreased the expression of Snail. Overall, these results suggested that EPHA4 may promote the motility and invasion of pancreatic cancer cells via the upregulation of MMP-2 and Snail, as well as the downregulation of E-cadherin. Thus, EPHA4 may act as a useful target for the treatment of pancreatic cancer.

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