TY - JOUR
T1 - Role of claudin proteins in regulating cancer stem cells and chemoresistance-potential implication in disease prognosis and therapy
AU - Gowrikumar, Saiprasad
AU - Singh, Amar B.
AU - Dhawan, Punita
N1 - Funding Information:
This study was supported by grant numbers BX002086 (VA merit) and CA216746 (NIH/NCI). Further funding came from a pilot project award from the Fred and Pamela Buffet Cancer Center, which was funded by a National Cancer Institute Cancer Center Support Grant, under award number P30 CA036727 to P.D., BX002761 (VA merit) to A.B.S., and Nebraska research initiative (NRI to P.D and A.B.S).
Publisher Copyright:
© 2019 by the authors. Licensee MDPI, Basel, Switzerland.
PY - 2020/1/1
Y1 - 2020/1/1
N2 - Claudins are cell–cell adhesion proteins, which are expressed in tight junctions (TJs), the most common apical cell-cell adhesion. Claudin proteins help to regulate defense and barrier functions, as well as differentiation and polarity in epithelial and endothelial cells. A series of studies have now reported dysregulation of claudin proteins in cancers. However, the precise mechanisms are still not well understood. Nonetheless, studies have clearly demonstrated a causal role of multiple claudins in the regulation of epithelial to mesenchymal transition (EMT), a key feature in the acquisition of a cancer stem cell phenotype in cancer cells. In addition, claudin proteins are known to modulate therapy resistance in cancer cells, a feature associated with cancer stem cells. In this review, we have focused primarily on highlighting the causal link between claudins, cancer stem cells, and therapy resistance. We have also contemplated the significance of claudins as novel targets in improving the efficacy of cancer therapy. Overall, this review provides a much-needed understanding of the emerging role of claudin proteins in cancer malignancy and therapeutic management.
AB - Claudins are cell–cell adhesion proteins, which are expressed in tight junctions (TJs), the most common apical cell-cell adhesion. Claudin proteins help to regulate defense and barrier functions, as well as differentiation and polarity in epithelial and endothelial cells. A series of studies have now reported dysregulation of claudin proteins in cancers. However, the precise mechanisms are still not well understood. Nonetheless, studies have clearly demonstrated a causal role of multiple claudins in the regulation of epithelial to mesenchymal transition (EMT), a key feature in the acquisition of a cancer stem cell phenotype in cancer cells. In addition, claudin proteins are known to modulate therapy resistance in cancer cells, a feature associated with cancer stem cells. In this review, we have focused primarily on highlighting the causal link between claudins, cancer stem cells, and therapy resistance. We have also contemplated the significance of claudins as novel targets in improving the efficacy of cancer therapy. Overall, this review provides a much-needed understanding of the emerging role of claudin proteins in cancer malignancy and therapeutic management.
KW - Cancer
KW - Chemoresistance
KW - Claudins
KW - Stem cell
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U2 - 10.3390/ijms21010053
DO - 10.3390/ijms21010053
M3 - Review article
C2 - 31861759
AN - SCOPUS:85076987461
SN - 1661-6596
VL - 21
JO - International Journal of Molecular Sciences
JF - International Journal of Molecular Sciences
IS - 1
M1 - 53
ER -