TY - JOUR
T1 - Drug resistance and Cancer stem cells
AU - Li, Yuan
AU - Wang, Zhenning
AU - Ajani, Jaffer A.
AU - Song, Shumei
N1 - Funding Information:
This work was supported by an MD Anderson Institutional Research Grant (3–0026317 to S. Song); and grants from Department of Defense (CA160433 and CA170906 to S. Song and CA160445 to J Ajani); and the National Institutes of Health (CA129906, CA138671, and CA172741 to J.A. Ajani).
Publisher Copyright:
© 2021, The Author(s).
PY - 2021/12
Y1 - 2021/12
N2 - Therapy resistance is a major problem when treating cancer patients as cancer cells develop mechanisms that counteract the effect of therapeutic compounds, leading to fit and more aggressive clones that contribute to poor prognosis. Therapy resistance can be both intrinsic and/or acquired. These are multifactorial events, and some are related to factors including adaptations in cancer stem cells (CSCs), epithelial-mesenchymal transition (EMT), deregulation of key signaling pathways, drug efflux through ABC transporters, acquired mutations, evading apoptosis, and activation of DNA damage response among others. Among these factors, CSCs represent the major source of therapy resistance. CSCs are a subset of tumor cells that are capable of self-renewal and multilineage progenitor expansion that are known to be intrinsically resistant to anticancer treatments. Multiple clones of CSCs pre-exist, and some can adopt and expand easily to changes in the tumor microenvironment (TME) and/or in response to radio- and chemotherapy. A combination of both intrinsic and extrinsic factors contributes to CSC-mediated therapy resistance. In this review, we will focus on CSCs and therapy resistance as well as suggest strategies to eliminate CSCs and, therefore, overcome resistance. [MediaObject not available: see fulltext.]
AB - Therapy resistance is a major problem when treating cancer patients as cancer cells develop mechanisms that counteract the effect of therapeutic compounds, leading to fit and more aggressive clones that contribute to poor prognosis. Therapy resistance can be both intrinsic and/or acquired. These are multifactorial events, and some are related to factors including adaptations in cancer stem cells (CSCs), epithelial-mesenchymal transition (EMT), deregulation of key signaling pathways, drug efflux through ABC transporters, acquired mutations, evading apoptosis, and activation of DNA damage response among others. Among these factors, CSCs represent the major source of therapy resistance. CSCs are a subset of tumor cells that are capable of self-renewal and multilineage progenitor expansion that are known to be intrinsically resistant to anticancer treatments. Multiple clones of CSCs pre-exist, and some can adopt and expand easily to changes in the tumor microenvironment (TME) and/or in response to radio- and chemotherapy. A combination of both intrinsic and extrinsic factors contributes to CSC-mediated therapy resistance. In this review, we will focus on CSCs and therapy resistance as well as suggest strategies to eliminate CSCs and, therefore, overcome resistance. [MediaObject not available: see fulltext.]
KW - Cancer stem cells
KW - Drug resistance
KW - EMT and TME
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U2 - 10.1186/s12964-020-00627-5
DO - 10.1186/s12964-020-00627-5
M3 - Review article
C2 - 33588867
AN - SCOPUS:85101427008
SN - 1478-811X
VL - 19
JO - Cell Communication and Signaling
JF - Cell Communication and Signaling
IS - 1
M1 - 19
ER -