Hypoxia-induced epithelial to mesenchymal transition in cancer

被引：114

作者：

Hapke, Robert Y. ^{[1
]}

Haake, Scott M. ^{[2
]}

机构：

[1] Vanderbilt Univ, 221 Kirkland Hall, Nashville, TN 37235 USA

[2] Vanderbilt Univ, Med Ctr, Dept Med, Div Hematol Oncol, Nashville, TN 37232 USA

来源：

CANCER LETTERS | 2020年 / 487卷

关键词：

EMT; Hypoxia; HIF; Metastasis; Immunosuppression; Cancer; NF-KAPPA-B; INDUCIBLE FACTOR 1-ALPHA; RENAL-CELL CARCINOMA; SUPERFAMILY SIGNALING PATHWAYS; UP-REGULATION; E-CADHERIN; HEPATOCELLULAR-CARCINOMA; TUMOR MICROENVIRONMENT; PANCREATIC-CANCER; TRANSCRIPTION FACTOR;

D O I：

10.1016/j.canlet.2020.05.012

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

A common feature of many solid tumors is low oxygen conditions due to inadequate blood supply. Hypoxia induces hypoxia inducible factor (HIF) stabilization and downstream signaling. This signaling has pleiotropic roles in cancers, including the promotion of cellular proliferation, changes in metabolism, and induction of angiogenesis. In addition, hypoxia is becoming recognized as an important driver of epithelial-to-mesenchymal (EMT) in cancer. During EMT, epithelial cells lose their typical polarized states and transition to a more mobile mesenchymal phenotype. Hypoxia induces this transition by modulating EMT signaling pathways, inducing EMT transcription factor activity, and regulating miRNA networks. As both hypoxia and EMT modulate the tumor microenvironment (TME) and are associated with immunosuppression, we also explore how these pathways may impact response to immuno-oncology therapeutics.

引用

页码：10 / 20

页数：11

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