Evaluating the effect of Alantolactone on the expression of N-cadherin and Vimentin genes effective in epithelial-mesenchymal transition (EMT) in breast cancer cell line (MDA-MB-231)

Abstract

ObjectiveBreast cancer is the second leading cause of death and the most common cancer among women. 10 to 20 percent of breast cancer samples have a negative triple phenotype that is more metastatic and more difficult to diagnose. Tumor invasion to other tissues and the formation of a secondary tumor depend on the epithelial to mesenchymal transition process, and the STAT3 pathway, which is associated with tumor proliferation and invasion and is the target gene for the drug, alantolactone. In this study, the EMT process is evaluated in negative triple-breasted cancer cells treated with alantolactone. MethodsWe used MDA-MB-231 cell line for assessing the survival rate of triple negative breast cancer cells and MTT test for determining alantolactone dose. We used three doses of 0.01 0.1, and 1 μM of alantolactone for evaluating the cell behavior in cancer invasion pathway. Real-time PCR was used to evaluate the expression of Vimentin, and N-cadherin genes. All of the tests were repeated thrice and the data were analyzed using Prism version 7.0. ResultsThe expression of Vimentin and N-cadherin decreased significantly at 1 μM alantolactone compared to the control group, p < 0.05. ConclusionAlantolactone affects the expression of Vimentin and N-cadherin through STAT3 signaling pathway and suppresses EMT process, metastasis and cancer invasion. This component may be used for treatment of patients with breast cancer.