TY - JOUR
T1 - Niche Modulation of IGF-1R Signaling
T2 - Its Role in Stem Cell Pluripotency, Cancer Reprogramming, and Therapeutic Applications
AU - Chen, Pei Chin
AU - Kuo, Yung Che
AU - Chuong, Cheng Ming
AU - Huang, Yen Hua
N1 - Funding Information:
The authors acknowledge the academic and science graphic illustration service provided by the Office of Research and Development at Taipei Medical University. This manuscript was edited by Wallace Academic Editing. Funding. This work was financially supported by research grants from the Ministry of Science and Technology, Taiwan (Grant numbers: MOST 107-2321-B-038-002, MOST 107-2314-B-038-061, MOST 108-2321-B-038-003, MOST109-2314-B-038-135, and MOST 109-2321-B-038-003); Health and Welfare Surcharge of Tobacco Products (Grant numbers: MOHW108-TDU-B-212-124014 and MOHW109-TDU-B-212-134014); Taipei Medical University (Grant number: TMU109-AE1-B02); Ministry of Education, Taiwan (Grant number: DP2-109-21121-01-T-03-02).
Publisher Copyright:
© Copyright © 2021 Chen, Kuo, Chuong and Huang.
Copyright:
Copyright 2021 Elsevier B.V., All rights reserved.
PY - 2021/1/12
Y1 - 2021/1/12
N2 - Stem cells work with their niches harmoniously during development. This concept has been extended to cancer pathology for cancer stem cells (CSCs) or cancer reprogramming. IGF-1R, a classical survival signaling, has been shown to regulate stem cell pluripotency, CSCs, or cancer reprogramming. The mechanism underlying such cell fate determination is unclear. We propose the determination is due to different niches in embryo development and tumor malignancy which modulate the consequences of IGF-1R signaling. Here we highlight the modulations of these niche parameters (hypoxia, inflammation, extracellular matrix), and the targeted stem cells (embryonic stem cells, germline stem cells, and mesenchymal stem cells) and CSCs, with relevance to cancer reprogramming. We organize known interaction between IGF-1R signaling and distinct niches in the double-sided cell fate with emerging trends highlighted. Based on these new insights, we propose that, through targeting IGF-1R signaling modulation, stem cell therapy and cancer stemness treatment can be further explored.
AB - Stem cells work with their niches harmoniously during development. This concept has been extended to cancer pathology for cancer stem cells (CSCs) or cancer reprogramming. IGF-1R, a classical survival signaling, has been shown to regulate stem cell pluripotency, CSCs, or cancer reprogramming. The mechanism underlying such cell fate determination is unclear. We propose the determination is due to different niches in embryo development and tumor malignancy which modulate the consequences of IGF-1R signaling. Here we highlight the modulations of these niche parameters (hypoxia, inflammation, extracellular matrix), and the targeted stem cells (embryonic stem cells, germline stem cells, and mesenchymal stem cells) and CSCs, with relevance to cancer reprogramming. We organize known interaction between IGF-1R signaling and distinct niches in the double-sided cell fate with emerging trends highlighted. Based on these new insights, we propose that, through targeting IGF-1R signaling modulation, stem cell therapy and cancer stemness treatment can be further explored.
KW - cancer stemness
KW - extracellular matrix
KW - hypoxia
KW - IGF-1R
KW - inflammation
KW - niche
KW - stem cells
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U2 - 10.3389/fcell.2020.625943
DO - 10.3389/fcell.2020.625943
M3 - Review article
AN - SCOPUS:85100040102
SN - 2296-634X
VL - 8
JO - Frontiers in Cell and Developmental Biology
JF - Frontiers in Cell and Developmental Biology
M1 - 625943
ER -
