Ls as a result of downregulation with the expression of glucose transporter (GLUT
Ls as a consequence of downregulation with the expression of glucose transporter (GLUT) PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/21994079 and MTMMP [83]. For resveratrol, studies have demonstrated its antimetastatic effect against a number of kinds of cancers by downregulation of MMP expression and its enzymatic activities, mainly MMP2 and MMP9. Among the sorts of cancer that resveratrol was active, we included glioblastoma [84], breast [85,86], a number of myeloma [99,87] and hepatocellular carcinoma [88]. 3.three. ECadherin The epithelial cell ell adhesion molecule cadherin , also known as epithelial cadherin (Ecadherin) is really a transmembrane glycoprotein that mediates cellcell adhesion via calciumdependent binding between two Ecadherin molecules at surface of adjacent cells [89,90]. Ecadherin is crucial for the epithelial cell behavior and evidence have shown that loss of its function is linked using the proliferation of several cancers, including lung [9], pancreatic [92], oral [93], liver [94], gastric [95], prostate [96] and ovarian [97]. The cellular function of Ecadherin is determined by the interaction using the catenin protein family, including , and p20 catenins [98]. catenin can be a important cytoplasmic protein that acts in association with catenin and creates a link between Ecadherin along with the actin cytoskeleton [89,99]. Chen and colleagues described the cell invasion and metastasis inhibitory activity of THS-044 site curcumin in a mice lung cancer [200]. Especially, curcumin upregulated the expression of Ecadherin by way of activation from the tumor suppressor DnaJlike heat shock protein 40 (HLJ), which has been linked with cell proliferation, invasion and metastasis against a number of human cancers [20]. The authors also recommended that curcumin modulates HLJ by enhancing the JNKJunD expression [200]. Further, the identical study group demonstrated the antimetastatic effect of curcumin against colorectal cancer cells using in vivo assays [202]. Curcumin played its activity by upregulation of Ecadherin expression top to an inhibition of mesenchymal transition (EMT). EMTrelated genes has been related with cancer progression and metastasis [203]. Likewise, not simply Ecadherin overexpression was observed for curcumin activity, but also the suppression of Sp transcriptional activity along with the inhibition of focal adhesion kinase (FAK) phosphorylation [202]. Curcumin was capable to block papillary thyroid cancer cells migration and invasion within a dual pathway, by increasing Ecadherin expression and inhibition of MMP9 activity [20406]. Zhang and coworkers have shown the potential application of curcumin in decreasing progression and metastasis of colon cancer cells by way of the overexpression of Ecadherin. Additionally, the authors demonstrated that others signaling pathways were involved, including downregulation of vimentin, inhibition of Wnt signaling pathway and downregulation of CXCR4 [207]. three.four. Protein Kinases Du and colleagues have reported the effect of curcumin inside the inhibition of cancer invasion and metastasis in human prostateassociated fibroblasts. Curcumin suppressed the MAOAmTORHIF signaling pathway thereby leading to a downregulation of reactive oxygen species (ROS), CXC chemokine receptor four (CXCR4) and interleukin6 (IL6) receptor, which has been linked to migration of prostate carcinoma cells [208]. The inhibition in the AktmTORP70S6K kinasesignaling pathway by curcumin was also reported in human melanoma cells. Curcumin decreased the phosphorylation of this kinasesignaling pathway top to an inhibition of.