期刊
BIOMEDICINE & PHARMACOTHERAPY
卷 141, 期 -, 页码 -出版社
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2021.111824
关键词
Paclitaxel; Docetaxel; Epithelial-to-mesenchymal transition (EMT); Drug resistance; Chemoresistance; Metastasis
资金
- Singapore Ministry of Education Tier 2 [MOE-T2EP30120-0016]
- National Medical Research Council of Singapore
- Singapore Ministry of Education under its Research Centers of Excellence initiative to Cancer Science Institute of Singapore
- National University of Singapore
EMT mechanism is responsible for cancer cell metastasis and migration, as well as drug resistance. Taxene chemotherapeutic agents PTX and DTX induce cancer cell cycle arrest by preventing microtubule depolymerization, while upstream mediators of EMT such as ZEB1/2 and TGF-ll affect cancer cells' response to these drugs.
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-ll, 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.
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