TY - JOUR
T1 - Cancer stem cell heterogeneity
T2 - Origin and new perspectives on CSC targeting
AU - Eun, Kiyoung
AU - Ham, Seok Won
AU - Kim, Hyunggee
N1 - Funding Information:
We are grateful to all members of the Cell Growth Regulation Laboratory for their helpful discussion. This work was supported by grants from the National Research Foundation (NRF) funded by the Ministry of Science, ICT and Future Planning (2015R1A5A1009024), from Next-Generation Biogreen21
PY - 2017
Y1 - 2017
N2 - Most of the cancers are still incurable human diseases. According to recent findings, especially targeting cancer stem cells (CSCs) is the most promising therapeutic strategy. CSCs take charge of a cancer hierarchy, harboring stem cell-like properties involving self-renewal and aberrant differentiation potential. Most of all, the presence of CSCs is closely associated with tumorigenesis and therapeutic resistance. Despite the numerous efforts to target CSCs, current anti-cancer therapies are still impeded by CSC-derived cancer malignancies; increased metastases, tumor recurrence, and even acquired resistance against the anti-CSC therapies developed in experimental models. One of the most forceful underlying reasons is a "cancer heterogeneity" due to "CSC plasticity". A comprehensive understanding of CSC-derived heterogeneity will provide novel insights into the establishment of efficient targeting strategies to eliminate CSCs. Here, we introduce findings on mechanisms of CSC reprogramming and CSC plasticity, which give rise to phenotypically varied CSCs. Also, we suggest concepts to improve CSC-targeted therapy in order to overcome therapeutic resistance caused by CSC plasticity and heterogeneity.
AB - Most of the cancers are still incurable human diseases. According to recent findings, especially targeting cancer stem cells (CSCs) is the most promising therapeutic strategy. CSCs take charge of a cancer hierarchy, harboring stem cell-like properties involving self-renewal and aberrant differentiation potential. Most of all, the presence of CSCs is closely associated with tumorigenesis and therapeutic resistance. Despite the numerous efforts to target CSCs, current anti-cancer therapies are still impeded by CSC-derived cancer malignancies; increased metastases, tumor recurrence, and even acquired resistance against the anti-CSC therapies developed in experimental models. One of the most forceful underlying reasons is a "cancer heterogeneity" due to "CSC plasticity". A comprehensive understanding of CSC-derived heterogeneity will provide novel insights into the establishment of efficient targeting strategies to eliminate CSCs. Here, we introduce findings on mechanisms of CSC reprogramming and CSC plasticity, which give rise to phenotypically varied CSCs. Also, we suggest concepts to improve CSC-targeted therapy in order to overcome therapeutic resistance caused by CSC plasticity and heterogeneity.
KW - Cancer
KW - Cancer stem cell
KW - Cancer therapy
KW - Plasticity
KW - Reprogramming
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U2 - 10.5483/BMBRep.2017.50.3.222
DO - 10.5483/BMBRep.2017.50.3.222
M3 - Short survey
C2 - 27998397
AN - SCOPUS:85016585968
VL - 50
SP - 117
EP - 125
JO - BMB Reports
JF - BMB Reports
SN - 1976-6696
IS - 3
ER -