期刊
CANCERS
卷 9, 期 8, 页码 -出版社
MDPI
DOI: 10.3390/cancers9080104
关键词
ovarian cancer; intraperitoneal metastasis; cadherins; heterogeneity; epithelial-to-mesenchymal transition (EMT); mesenchymal-to-epithelial transition (MET); intraperitoneal tumor microenvironment; computational modeling of EMT
类别
资金
- National Institutes of Health/National Cancer Institute [RO1CA109545, RO1CA086984]
- Leo and Anne Albert Charitable Trust
- Research Like a Champion grant
- Walther Cancer Foundation Seeding Research in Cancer grant
- Scientist Development Grant from American Heart Association [SDG33680177]
Unlike most epithelial malignancies which metastasize hematogenously, metastasis of epithelial ovarian cancer (EOC) occurs primarily via transcoelomic dissemination, characterized by exfoliation of cells from the primary tumor, avoidance of detachment-induced cell death (anoikis), movement throughout the peritoneal cavity as individual cells and multi-cellular aggregates (MCAs), adhesion to and disruption of the mesothelial lining of the peritoneum, and submesothelial matrix anchoring and proliferation to generate widely disseminated metastases. This exceptional microenvironment is highly permissive for phenotypic plasticity, enabling mesenchymal-to-epithelial (MET) and epithelial-to-mesenchymal (EMT) transitions. In this review, we summarize current knowledge on EOC heterogeneity in an EMT context, outline major regulators of EMT in ovarian cancer, address controversies in EMT and EOC chemoresistance, and highlight computational modeling approaches toward understanding EMT/MET in EOC.
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