Breast tumor and stromal cell responses to TGF-β and hypoxia in matrix deposition.
Breast tumor and stromal cell responses to TGF-β and hypoxia in matrix deposition.
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DOI：
10.1016/j.matbio.2012.11.016
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发表时间：
2013-03-11
期刊：
影响因子：
6.9
通讯作者：
Keely, Patricia J.
中科院分区：
文献类型：
--
作者：
Curran, Colleen S.;Keely, Patricia J.
组成细胞外基质（ECM）的成分是正常组织稳态以及乳腺肿瘤发展和进展的组成部分。ECM的分泌、构建和重塑各自由肿瘤细胞、成纤维细胞和巨噬细胞之间的复杂相互作用调节。转化生长因子-β（Transforming growth factor-β，TGF-β）是调节细胞产生ECM分子以及细胞与ECM粘附相互作用的重要分子。此外，缺氧细胞信号，引发缺氧，额外的代谢因子或受体活化，与ECM的形成和乳腺癌的进展。TGF-β和缺氧细胞信号都涉及癌相关成纤维细胞和肿瘤相关巨噬细胞的功能和形态变化。此外，响应于缺氧诱导的趋化因子的肿瘤和基质细胞的增强的募集导致ECM沉积和重塑增加、血管形成增加和肿瘤迁移增强。因此，阐明肿瘤和基质细胞之间响应于TGF-β和缺氧的组合信号的协作网络可以产生对靶向肿瘤和基质细胞的治疗参数的了解。
The components that comprise the extracellular matrix (ECM) are integral to normal tissue homeostasis as well as the development and progression of breast tumors. The secretion, construction, and remodeling of the ECM are each regulated by a complex interplay between tumor cells, fibroblasts and macrophages. Transforming growth factor-β (TGF-β) is an essential molecule in regulating the cellular production of ECM molecules and the adhesive interactions of cells with the ECM. Additionally, hypoxic cell signals, initiated by oxygen deprivation, additional metabolic factors or receptor activation, are associated with ECM formation and the progression of breast cancer. Both TGF-β and hypoxic cell signals are implicated in the functional and morphological changes of cancer-associated-fibroblasts and tumor-associated-macrophages. Moreover, the enhanced recruitment of tumor and stromal cells in response to hypoxia-induced chemokines leads to increased ECM deposition and remodeling, increased blood vessel formation, and enhanced tumor migration. Thus, elucidation of the collaborative networks between tumor and stromal cells in response to the combined signals of TGF-β and hypoxia may yield insight into treatment parameters that target both tumor and stromal cells.
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