Xiao-Ai-Ping(XAP),a traditional oriental medicinal herb isolated from the stem of Marsdenia tenacissima(Roxb.)Wight et Arn.,has been shown to induce tumor cell apoptosis.In this study,we used confocal fluorescence mic...Xiao-Ai-Ping(XAP),a traditional oriental medicinal herb isolated from the stem of Marsdenia tenacissima(Roxb.)Wight et Arn.,has been shown to induce tumor cell apoptosis.In this study,we used confocal fluorescence microscopy and fluorescence resonance energy transfer(FRET)techniques to study the molecular mechanism of XAPinduced apoptosis in single living human lung adenocarcinoma(ASTC-a-1)cells.The efficacious apoptosis was observed at 6 h after of 100μl XAP treatment.Further monitoring the dynamics of caspase-3 activation using FRET imaging in single living ASTC-a-1 cell expressing stably with SCAT3,a FRET probe,showed that XAP activated the caspase-3 at about 2 h after XAP treatment.These data suggest that caspase-3 activation was involved in the XAP-induced apoptosis in ASTC-a-1 cells.展开更多
Marsdenia tenacissima, a traditional Chinese medicine, is long been used to treat various diseases including asthma, cancer, trachitis, tonsillitis, pharyngitis, cystitis, and pneumonia. Although Marsdenia tenacissima...Marsdenia tenacissima, a traditional Chinese medicine, is long been used to treat various diseases including asthma, cancer, trachitis, tonsillitis, pharyngitis, cystitis, and pneumonia. Although Marsdenia tenacissima has been demonstrated to have strong anti-tumor effects against primary tumors, its effect on cancer metastasis remains to be defined, and the molecular mechanism underlying the anti-metastatic effect is unknown. In the present study, we investigated the effects of XAP(an extract of Marsdenia tenacissima) on A549 lung cancer cell migration and explored the role of CCR5-CCL5 axis in the anti-metastatic effects of XAP. Our resutls showed that XAP inhibited A549 lung cancer cell migration and invasion in a dose-dependent manner. The protein levels of CCR5, but not CCR9 and CXCR4, were decreased by XAP. The secretion of CCL5, the ligand of CCR5, was reduced by XAP. XAP down-regulated Rho C expression and FAK phosphorylation. In conclusion, XAP inhibited A549 cell migration and invasion through down-regulation of CCR5-CCL5 axis, Rho C, and FAK.展开更多
基金supported by National Natural Science Foundation of China(Grant No.30670507)the Opening Project of MOE Key laboratory of Laser Life Science,South China Normal University,Guangzhou 510631,China.
文摘Xiao-Ai-Ping(XAP),a traditional oriental medicinal herb isolated from the stem of Marsdenia tenacissima(Roxb.)Wight et Arn.,has been shown to induce tumor cell apoptosis.In this study,we used confocal fluorescence microscopy and fluorescence resonance energy transfer(FRET)techniques to study the molecular mechanism of XAPinduced apoptosis in single living human lung adenocarcinoma(ASTC-a-1)cells.The efficacious apoptosis was observed at 6 h after of 100μl XAP treatment.Further monitoring the dynamics of caspase-3 activation using FRET imaging in single living ASTC-a-1 cell expressing stably with SCAT3,a FRET probe,showed that XAP activated the caspase-3 at about 2 h after XAP treatment.These data suggest that caspase-3 activation was involved in the XAP-induced apoptosis in ASTC-a-1 cells.
基金supported by the National Natural Science Foundation of China(No.81302794)the Natural Science Foundation of Jiangsu Province(No.2012353)the Specialized Research Fund for the Doctoral Program of Higher Education of China(No.20120096120012)
文摘Marsdenia tenacissima, a traditional Chinese medicine, is long been used to treat various diseases including asthma, cancer, trachitis, tonsillitis, pharyngitis, cystitis, and pneumonia. Although Marsdenia tenacissima has been demonstrated to have strong anti-tumor effects against primary tumors, its effect on cancer metastasis remains to be defined, and the molecular mechanism underlying the anti-metastatic effect is unknown. In the present study, we investigated the effects of XAP(an extract of Marsdenia tenacissima) on A549 lung cancer cell migration and explored the role of CCR5-CCL5 axis in the anti-metastatic effects of XAP. Our resutls showed that XAP inhibited A549 lung cancer cell migration and invasion in a dose-dependent manner. The protein levels of CCR5, but not CCR9 and CXCR4, were decreased by XAP. The secretion of CCL5, the ligand of CCR5, was reduced by XAP. XAP down-regulated Rho C expression and FAK phosphorylation. In conclusion, XAP inhibited A549 cell migration and invasion through down-regulation of CCR5-CCL5 axis, Rho C, and FAK.
