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Title: New insight towards development of paclitaxel and docetaxel resistance in cancer cells: EMT as a novel molecular mechanism and therapeutic possibilities
Authors: Ashrafizadeh, Milad
Mirzaei, Sepideh
Hashemi, Farid
Zarrabi, Ali
Zabolian, Amirhossein
Saleki, Hossein
Sharifzadeh, Seyed Omid
Soleymani, Leyla
Daneshi, Salman
Hushmandi, Kiavash
Khan, Haroon
Kumar, Alan Prem 
Aref, Amir Reza
Samarghandian, Saeed
Keywords: Chemoresistance
Drug resistance
Epithelial-to-mesenchymal transition (EMT)
Issue Date: 1-Sep-2021
Publisher: Elsevier Masson s.r.l.
Citation: Ashrafizadeh, Milad, Mirzaei, Sepideh, Hashemi, Farid, Zarrabi, Ali, Zabolian, Amirhossein, Saleki, Hossein, Sharifzadeh, Seyed Omid, Soleymani, Leyla, Daneshi, Salman, Hushmandi, Kiavash, Khan, Haroon, Kumar, Alan Prem, Aref, Amir Reza, Samarghandian, Saeed (2021-09-01). New insight towards development of paclitaxel and docetaxel resistance in cancer cells: EMT as a novel molecular mechanism and therapeutic possibilities. Biomedicine and Pharmacotherapy 141 : 111824. ScholarBank@NUS Repository.
Rights: Attribution-NonCommercial-NoDerivatives 4.0 International
Abstract: Epithelial-to-mesenchymal transition (EMT) mechanism is responsible for metastasis and migration of cancer cells to neighboring cells and tissues. Morphologically, epithelial cells are transformed to mesenchymal cells, and at molecular level, E-cadherin undergoes down-regulation, while an increase occurs in N-cadherin and vimentin levels. Increasing evidence demonstrates role of EMT in mediating drug resistance of cancer cells. On the other hand, paclitaxel (PTX) and docetaxel (DTX) are two chemotherapeutic agents belonging to taxene family, capable of inducing cell cycle arrest in cancer cells via preventing microtubule depolymerization. Aggressive behavior of cancer cells resulted from EMT-mediated metastasis can lead to PTX and DTX resistance. Upstream mediators of EMT such as ZEB1/2, TGF-?, microRNAs, and so on are involved in regulating response of cancer cells to PTX and DTX. Tumor-suppressing factors inhibit EMT to promote PTX and DTX sensitivity of cancer cells. Furthermore, three different strategies including using anti-tumor compounds, gene therapy and delivery systems have been developed for suppressing EMT, and enhancing cytotoxicity of PTX and DTX against cancer cells that are mechanistically discussed in the current review. © 2021
Source Title: Biomedicine and Pharmacotherapy
ISSN: 0753-3322
DOI: 10.1016/j.biopha.2021.111824
Rights: Attribution-NonCommercial-NoDerivatives 4.0 International
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