ZHU Zhi-jie, LIU Zhao-guo, ZHOU Liang, et al. Anti-metastatic Effect of Cryptotanshinone on MDA-MB-231 Breast Cancer and Its Underlying Mechanism[J]. Chinese journal of experimental traditional medical formulae, 2014, 20(11): 160-165.
ZHU Zhi-jie, LIU Zhao-guo, ZHOU Liang, et al. Anti-metastatic Effect of Cryptotanshinone on MDA-MB-231 Breast Cancer and Its Underlying Mechanism[J]. Chinese journal of experimental traditional medical formulae, 2014, 20(11): 160-165. DOI: 10.13422/j.cnki.syfix.2014110160.
Objective:To investigate the anti-metastatic effect of cryptotanshinone on human breast cancer and its possible mechanisms. Method:The ability of cryptotanshinone on proliferation was detected after labeling with bromodeoxyuridine(BrdU) by immunofluorescence staining. We furher used wound healing assay and Transwell migration assay to investigate the effect of cryptotanshinone on cell mobility in vitro. Western blot was used to measure the protein expression related to epithelial mesenchymal transition(EMT). Effect of cryptotanshinone on nuclear factor(NF)-κB transcriptional activity was detected by Dual-Luciferase gene reporter assay system. Furthermore
we used transgenic zebrafish tumor model to illustrate the anti-metastatic effect of cryptotanshinone in vivo. Result:Cryptotanshinone showed a great inhibitory ability on cell proliferation and migration in vitro. Cryptotanshinone also does-dependently increased the expression of E-cadherin but decreased the expression of N-cadherin. The transcriptional activity of NF-κB was prohibited by cryptotanshinone as well. Moreover
cryptotanshinone inhibited MDA-MB-231 tumor metastasis in a dose dependent manner in zebrafish embyos by decreasing the number of disseminated foci from tumor mass as well as maximal distance of metastasis. Conclusion:Cryptotanshinone showed both anti-metastatic effect in vivo and in vitro. The proliferation of MDA-MB-231 was also inhibited by cryptotanshinone. The underlying anti-metastatic mechanism of cryptotanshinone on MDA-MB-231 breast cancer cells involved reversion of EMT via downregulating transcriptional activity of NF-κB.