期刊
FREE RADICAL BIOLOGY AND MEDICINE
卷 79, 期 -, 页码 269-280出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2014.11.020
关键词
Tumor microenvironment; Tumor metabolism; Mechanosignaling; Cancer; ECM stiffness; Free radicals
资金
- National Institutes of Health [NHLBI T32 HL007544, F32 CA174319, R01 CA155664, R01 CA158668, R01 CA170851, R01 CA136590, R01 CA114462, R01 CA142833]
- NIBIB [R21 EB008811, U54CA163155-01, U54CA143836, CA138818-01A1, R01 CA174929, R33 CA183685-01, U01 ES019458]
- Susan G. Komen Breast Cancer Award [KG091020, KG110560PP]
- V-Foundation Award
- CDMRP Breast Cancer Research Program [BC074970]
- Era of Hope Scholar Expansion [W81XWH-13-1-0216]
Desmosplasia is a characteristic of most solid tumors and leads to fibrosis through abnormal extracellular matrix (ECM) deposition, remodeling, and posttranslational modifications. The resulting stiff tumor Aroma not only compromises vascular integrity to induce hypoxia and impede drug delivery, but also promotes aggressiveness by potentiating the activity of key growth, invasion, and survival pathways. Intriguingly, many of the protumorigenic signaling pathways that are mechanically activated by ECM stiffness also promote glucose uptake and aerobic glycolysis, and an altered metabolism is a recognized hallmark of cancer. Indeed, emerging evidence suggests that metabolic alterations and an abnormal ECM may cooperatively drive cancer cell aggression and treatment resistance. Accordingly, improved methods to monitor tissue mechanics and metabolism promise to improve diagnostics and treatments to ameliorate ECM stiffening and elevated mechanosignaling may improve patient outcome. Here we discuss the interplay between ECM mechanics and metabolism in tumor biology and suggest that monitoring these processes and targeting their regulatory pathways may improve diagnostics, therapy, and the prevention of malignant transformation. (C) 2014 Elsevier Inc. All rights reserved.
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