An overview of extracellular matrix and its remodeling in the development of cancer and metastasis with a glance at therapeutic approaches

被引:6
|
作者
Afshar, Kimiya [1 ]
Sanaei, Mohammad-Javad [1 ]
Ravari, Mehrnaz Sadat [2 ]
Pourbagheri-Sigaroodi, Atieh [1 ]
Bashash, Davood [1 ]
机构
[1] Shahid Beheshti Univ Med Sci, Sch Allied Med Sci, Dept Hematol & Blood Banking, Tehran, Iran
[2] Kerman Univ Med Sci, Res Ctr Hydatid Dis Iran, Kerman, Iran
关键词
cancer; extracellular matrix; integrin; matrix targeting; matrix turnover; metastasis; CELL-MIGRATION; LYSYL OXIDASE; TISSUE TRANSGLUTAMINASE; TUMOR MICROENVIRONMENT; CHEMOTHERAPY RESPONSE; FUNCTIONAL DIVERSITY; GENE-EXPRESSION; TGF-BETA; COLLAGEN; FIBROSIS;
D O I
10.1002/cbf.3846
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The extracellular matrix (ECM) is an inevitable part of tissues able to provide structural support for cells depending on the purpose of tissues and organs. The dynamic characteristics of ECM let this system fluently interact with the extrinsic triggers and get stiffed, remodeled, and/or degraded ending in maintaining tissue homeostasis. ECM could serve as the platform for cancer progression. The dysregulation of biochemical and biomechanical ECM features might take participate in some pathological conditions such as aging, tissue destruction, fibrosis, and particularly cancer. Tumors can reprogram how ECM remodels by producing factors able to induce protein synthesis, matrix proteinase expression, degradation of the basement membrane, growth signals and proliferation, angiogenesis, and metastasis. Therefore, targeting the ECM components, their secretion, and their interactions with other cells or tumors could be a promising strategy in cancer therapies. The present study initially introduces the physiological functions of ECM and then discusses how tumor-dependent dysregulation of ECM could facilitate cancer progression and ends with reviewing the novel therapeutic strategies regarding ECM. Extracellular matrix (ECM) is a dynamic network consisting of collagens, proteoglycans, and glycoproteins.ECM acts as a physical barrier, an anchor, and a signal transducer in the homeostasis.By boosting cell signaling, dense ECM induces tumor growth, survival, and migration.Targeting ECM components and their producers (cancer-associated fibroblasts) hasn't yielded promising outcomes.
引用
收藏
页码:930 / 952
页数:23
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