Mitochondrial SOD2 regulates epithelial–mesenchymal transition and cell populations defined by differential CD44 expression

• Published in: Oncogene Vol. 34; no. 41; pp. 5229 - 5239
• Main Authors: Kinugasa, H, Whelan, K A, Tanaka, K, Natsuizaka, M, Long, A, Guo, A, Chang, S, Kagawa, S, Srinivasan, S, Guha, M, Yamamoto, K, St Clair, D K, Avadhani, N G, Diehl, J A, Nakagawa, H
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 08.10.2015; Nature Publishing Group
• Subjects: 13; 13/31; 38/109; 38/89; 631/67/327; Antioxidants; Apoptosis; Cancer; CD44 antigen; Cell Biology; Cell death; Cell Line; Cellular biology; Epithelial cells; Epithelial-Mesenchymal Transition; Esophagus; Flow cytometry; Gene expression; Gene Expression Regulation, Enzymologic; Gene regulation; Genetic aspects; Genetic engineering; Health aspects; Homeodomain Proteins - metabolism; Human Genetics; Humans; Hyaluronan Receptors; Immune response; Internal Medicine; Keratinocytes; Medicine; Medicine & Public Health; Mesenchyme; Metastases; Metastasis; Mitochondria; Mitochondria - enzymology; NF-kappa B - metabolism; NF-κB protein; Oncology; original-article; Phenotypes; Properties; Reactive oxygen species; Repressor Proteins - metabolism; Ribonucleic acid; RNA; RNA-mediated interference; Senescence; Superoxide dismutase; Superoxide Dismutase - physiology; Transcription; Zinc Finger E-box Binding Homeobox 2

Epithelial–mesenchymal transition (EMT) promotes cancer cell invasion, metastasis and treatment failure. EMT may be activated in cancer cells by reactive oxygen species (ROS). EMT may promote conversion of a subset of cancer cells from a CD44 low -CD24 high (CD44L) epithelial phenotype to a CD44 hig...