Fig_5.tif (788.22 kB)
Schematic model of the signaling pathways involved in chrysin inhibiting PMA-induced MMP-9 expression.
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posted on 2015-04-15, 02:44 authored by Yong Xia, Sen Lian, Pham Ngoc Khoi, Hyun Joong Yoon, Young Eun Joo, Kee Oh Chay, Kyung Keun Kim, Young Do JungPMA stimulates ERK1/2 and JNK1/2 phosphorylation, in turn activating c-Fos and c-Jun, respectively. The phosphorylated c-Fos and c-Jun are translated into the nucleus, where they cooperatively bind to AP-1 binding site, thereby triggering MMP-9 gene expression. The higher level of MMP-9 expression enhances the degradation of the matrix and increases the cell invasiveness. In this model, chrysin acts as an inhibitor of the JNK1/2 and ERK1/2 signaling pathways, and decreases PMA-induced MMP-9 via suppressing AP-1 activation.
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anticancer effectGastric Cancer Cells Cell invasionBlocking APcancer cell invasion processtumor aggressivenessdecoy oligodeoxynucleotidesHigh expression levelscancer cellscancer AGS cellschrysinpmacancer metastasisAGS cells pretreatedmmptranscriptional factorpromoter studyerktumor metastasisJNK Pathways
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