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Cancer stem cells and epithelial‐mesenchymal transition: Novel therapeutic targets for cancer
Author(s) -
Ishiwata Toshiyuki
Publication year - 2016
Publication title -
pathology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
eISSN - 1440-1827
pISSN - 1320-5463
DOI - 10.1111/pin.12447
Subject(s) - cancer stem cell , cancer research , epithelial–mesenchymal transition , metastasis , cancer cell , cancer , mesenchymal stem cell , stromal cell , pancreatic cancer , cd44 , biology , nestin , pathology , stem cell , medicine , cell , microbiology and biotechnology , genetics , neural stem cell
Despite the development of various therapeutic approaches, recurrence and metastasis remain major problems for patients with advanced cancer. Recent studies have shown that cancer stem cells (CSCs) play an important role in cancer aggressiveness. In cancer tissues, a small number of CSCs are able to self‐renew and differentiate into heterogeneous cancer cells. CSCs usually remain in the resting phase of the cell cycle and possess efficient drug efflux pathways. Thus, they are resistant to chemoradiotherapy and surviving CSCs contribute to recurrence. During cancer metastasis, CSCs undergo epithelial–mesenchymal transition (EMT), thereby acquiring mesenchymal features, migrating to adjacent stromal tissues, and invading blood or lymph vessels. Recent studies showed that EMT‐inducible factors also enhance or induce CSC‐like features in cancer cells. These findings suggest that EMT is closely correlated with cancer recurrence and metastasis. Inhibition of nestin, a CSC marker, reduces the aggressiveness of several types of cancer. Suppression of the mesenchymal variant of fibroblast growth factor (FGFR)‐2, FGFR‐2 IIIc, and regulation of the EMT using epithelial splicing regulatory protein 1 (ESRP1) are effective in the treatment of immunodeficient mice with pancreatic cancer. The roles of CSCs and EMT in cancer and possible therapies are discussed in this review.