Epithelial-mesenchymal transition(EMT)is a natural phenomenon thatoccurs during embryodevelopment.It is a phenomenon involving the transition of adherence-dependent stationary epithelial cells to adherence-independent...Epithelial-mesenchymal transition(EMT)is a natural phenomenon thatoccurs during embryodevelopment.It is a phenomenon involving the transition of adherence-dependent stationary epithelial cells to adherence-independent migratory mesenchymal cells.Tumours reactivate this machinery and evade anti-tumour immunity and inhibition by cancer-specific drugs.EMT harnesses complex crosstalk among cancer cell signalling pathways that make it difficult to tackle therapeutically,and it plays a pivotal role in cancer metastasis.Most screening platforms and approved drugs are limited by their applicability to epithelial cancers.There is a significant need for developing new strategies targeting metastatic cancers.Here,we review the challenges with the current methods of screening and available drugs for EMT and shed some light on the key essentials needed for next-generation drug discovery attempts.展开更多
Cancer stem cells have become the new target of chemotherapy with specific cell marker. CD133 is shown to be highly expressed in glioma cancer stem cells. In this study, a drug delivery system is designed to target CD...Cancer stem cells have become the new target of chemotherapy with specific cell marker. CD133 is shown to be highly expressed in glioma cancer stem cells. In this study, a drug delivery system is designed to target CD133 by a seven amino acid peptide （TR peptide）, which is capable to specifically bind to CD 133. First, TR was conjugated to DSPE-PEG and coumarin-6 was loaded into the DSPE-PEG micelles. Then fluorescence-activated cell sorting （FACS） and tumorsphere culture were conducted to isolate cancer stern cells in C6 cells. The enhanced uptake of micelles was observed by confocal microscopy and flow cytometry, suggesting that TR peptide-modified micelles may exhibit better anti-cancer efficacy by targeting CD133^＋ glioma stem cells.In conclusion, TR peptide-modified micelles may provide new strategy to achieve enhanced specificity to CD 133^＋ glioma stem cells.展开更多
文摘Epithelial-mesenchymal transition(EMT)is a natural phenomenon thatoccurs during embryodevelopment.It is a phenomenon involving the transition of adherence-dependent stationary epithelial cells to adherence-independent migratory mesenchymal cells.Tumours reactivate this machinery and evade anti-tumour immunity and inhibition by cancer-specific drugs.EMT harnesses complex crosstalk among cancer cell signalling pathways that make it difficult to tackle therapeutically,and it plays a pivotal role in cancer metastasis.Most screening platforms and approved drugs are limited by their applicability to epithelial cancers.There is a significant need for developing new strategies targeting metastatic cancers.Here,we review the challenges with the current methods of screening and available drugs for EMT and shed some light on the key essentials needed for next-generation drug discovery attempts.
基金The Key Program of National Science Foundation(Grant No.81130059)the National Basic Research Program of China(Grant No.973 program,2013CB932501)
文摘Cancer stem cells have become the new target of chemotherapy with specific cell marker. CD133 is shown to be highly expressed in glioma cancer stem cells. In this study, a drug delivery system is designed to target CD133 by a seven amino acid peptide （TR peptide）, which is capable to specifically bind to CD 133. First, TR was conjugated to DSPE-PEG and coumarin-6 was loaded into the DSPE-PEG micelles. Then fluorescence-activated cell sorting （FACS） and tumorsphere culture were conducted to isolate cancer stern cells in C6 cells. The enhanced uptake of micelles was observed by confocal microscopy and flow cytometry, suggesting that TR peptide-modified micelles may exhibit better anti-cancer efficacy by targeting CD133^＋ glioma stem cells.In conclusion, TR peptide-modified micelles may provide new strategy to achieve enhanced specificity to CD 133^＋ glioma stem cells.
