WIN 55,212-2 Inhibits the Epithelial Mesenchymal Transition of Gastric Cancer Cells via COX-2 Signals
| Autor: | Chengrong Wu, Jun Cui, Zhihua Wang, Xiang-Shu Xian, Liuye Huang, Bo Zhang |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Epithelial-Mesenchymal Transition Physiology Morpholines Down-Regulation Vimentin Biology Naphthalenes lcsh:Physiology lcsh:Biochemistry 03 medical and health sciences Phosphatidylinositol 3-Kinases 0302 clinical medicine Downregulation and upregulation Cell Movement Stomach Neoplasms Cell Line Tumor WIN 55 212-2 medicine Humans Neoplasm Invasiveness lcsh:QD415-436 Epithelial–mesenchymal transition Phosphorylation Protein kinase B lcsh:QP1-981 EMT Cell migration COX-2 Benzoxazines Up-Regulation Gene Expression Regulation Neoplastic 030104 developmental biology Cell culture Cyclooxygenase 2 030220 oncology & carcinogenesis Cancer cell Immunology Cancer research biology.protein Gastric cancer Proto-Oncogene Proteins c-akt medicine.drug Signal Transduction |
| Zdroj: | Cellular Physiology and Biochemistry, Vol 39, Iss 6, Pp 2149-2157 (2016) |
| ISSN: | 1421-9778 1015-8987 |
| Popis: | Background: Cannabinoids (the active components of Cannabis sativa) and their derivatives have received considerable interest due to reports that they can affect the tumor growth, migration, and metastasis. Previous studies showed that the cannabinoid agonist WIN 55,212-2 (WIN) was associated with gastric cancer (GC) metastasis, but the mechanisms were unknown. Methods: The effects of WIN on GC cell migration and invasion were analyzed by the wound-healing assay and Transwell assay. Quantitative real-time PCR and Western blot were used to evaluate changes in expression of COX-2 and EMT associated markers in SGC7901 and AGS cells. Results: WIN inhibited cell migration, invasion, and epithelial to mesenchymal transition (EMT) in GC. WIN treatment resulted in the downregulation of cyclooxygenase-2 (COX-2) expression and decreased the phosphorylation of AKT, and inhibited EMT in SGC7901 cells. Decreased expression of COX-2 and vimentin, and increased expression of E-cadherin, which was induced by WIN, were normalized by overexpression of AKT, suggesting that AKT mediated, at least partially, the WIN suppressed EMT of GC cells. Conclusion: WIN can inhibit the EMT of GC cells through the downregulation of COX-2. |
| Databáze: | OpenAIRE |
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