Abstract
Epithelial–mesenchymal transition (EMT) is known to play an important role in cancer progression, metastasis and drug resistance. Although there are controversies surrounding the causal relationship between EMT and cancer metastasis, the role of EMT in cancer drug resistance has been increasingly recognized. Numerous EMT-related signaling pathways are involved in drug resistance in cancer cells. Cells undergoing EMT show a feature similar to cancer stem cells (CSCs), such as an increase in drug efflux pumps and anti-apoptotic effects. Therefore, targeting EMT has been considered a novel opportunity to overcome cancer drug resistance. This review describes the mechanism by which EMT contributes to drug resistance in cancer cells and summarizes new advances in research in EMT-associated drug resistance.
Highlights
Cancer is one of the leading causes of human death
More than 100 targeted cancer therapy drugs have been approved for cancer patients and much more are in clinical investigations
In the control group of mice, most of the lung metastasized cancer cells had not undergone epithelial–mesenchymal transition (EMT), while chemotherapy treated mice had significantly larger number of EMT cancer cells in lung metastatic region. These data suggested that EMT plays an important role in cancer drug resistance and contributes to metastasis after chemotherapy treatment
Summary
Cancer is one of the leading causes of human death. Despite significant advances in cancer research throughout the decades, treatment of cancer is still facing serious challenges. Chemotherapy is one of the well-established types of cancer treatment and has long been used as monotherapy or in combination with surgery or radiotherapy to treat cancer patients. Chemotherapy drugs, both classical cytotoxic drugs and molecular targeted drugs, have been challenged by drug resistance, a major cause of cancer treatment failure and cancer-related mortality. While many of the targeted therapy drugs showed promising early clinical outcomes with improved overall survival, a large number of the patients receiving targeted therapy developed drug resistance after long-term drug administration [1]. More than 100 targeted cancer therapy drugs have been approved for cancer patients and much more are in clinical investigations.
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