期刊
FRONTIERS IN ONCOLOGY
卷 12, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fonc.2022.1052457
关键词
cancer; insulin-like growth factor binding protein 5 (IGFBP5); tumor microenvironment (TME); insulin-like growth factor (IGF); extracellular matrix (ECM); therapy resistance
类别
资金
- National Institute on Minority Health and Health Disparities at the NIH
- [U54MD012397]
This review discusses the different roles of IGF signaling and IGFBP5 in disease, emphasizing the need to clarify the IGF-independent actions of IGFBP5, the impact of its subcellular localization, the differential activities of each subdomain, and the response to elements of the tumor microenvironment (TME). Recent advances addressing the role of IGFBP5 in resistance to cancer therapeutics are also discussed.
Insulin-like growth factor binding proteins (IGFBPs) and the associated signaling components in the insulin-like growth factor (IGF) pathway regulate cell differentiation, proliferation, apoptosis, and adhesion. Of the IGFBPs, insulin-like growth factor binding protein 5 (IGFBP5) is the most evolutionarily conserved with a dynamic range of IGF-dependent and -independent functions, and studies on the actions of IGFBP5 in cancer have been somewhat paradoxical. In cancer, the IGFBPs respond to external stimuli to modulate disease progression and therapeutic responsiveness in a context specific manner. This review discusses the different roles of IGF signaling and IGFBP5 in disease with an emphasis on discoveries within the last twenty years, which underscore a need to clarify the IGF-independent actions of IGFBP5, the impact of its subcellular localization, the differential activities of each of the subdomains, and the response to elements of the tumor microenvironment (TME). Additionally, recent advances addressing the role of IGFBP5 in resistance to cancer therapeutics will be discussed. A better understanding of the contexts in which IGFBP5 functions will facilitate the discovery of new mechanisms of cancer progression that may lead to novel therapeutic opportunities
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据