EMT-activating transcription factors in cancer: beyond EMT and tumor invasiveness

被引:0
作者
Ester Sánchez-Tilló
Yongqing Liu
Oriol de Barrios
Laura Siles
Lucia Fanlo
Miriam Cuatrecasas
Douglas S. Darling
Douglas C. Dean
Antoni Castells
Antonio Postigo
机构
[1] IDIBAPS,Group of Transcriptional Regulation of Gene Expression, Department of Oncology and Hematology
[2] IDIBAPS,CIBERehd (Gastrointestinal and Pancreatic Oncology)
[3] Louisville Health Science Center,James Graham Brown Cancer Center
[4] Louisville Health Science Center,Department of Ophthalmology and Birth Defects Center
[5] University Pompeu Fabra,Master Program in Biomedical Research
[6] Hospital Clinic and IDIBAPS’ Tumor Bank,Department of Pathology
[7] University of Louisville,Department of Oral Health and Rehabilitation, Center for Genetics and Molecular Medicine
[8] Hospital Clinic,Institute of Digestive and Metabolic Diseases
[9] ICREA,undefined
来源
Cellular and Molecular Life Sciences | 2012年 / 69卷
关键词
Cancer stem cells; E-cadherin; EMT; Invasiveness; Metastasis; Snail1; Snail2; Tumorigenesis; Twist1; Twist2; ZEB1; ZEB2;
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摘要
Cancer is a complex multistep process involving genetic and epigenetic changes that eventually result in the activation of oncogenic pathways and/or inactivation of tumor suppressor signals. During cancer progression, cancer cells acquire a number of hallmarks that promote tumor growth and invasion. A crucial mechanism by which carcinoma cells enhance their invasive capacity is the dissolution of intercellular adhesions and the acquisition of a more motile mesenchymal phenotype as part of an epithelial-to-mesenchymal transition (EMT). Although many transcription factors can trigger it, the full molecular reprogramming occurring during an EMT is mainly orchestrated by three major groups of transcription factors: the ZEB, Snail and Twist families. Upregulated expression of these EMT-activating transcription factors (EMT-ATFs) promotes tumor invasiveness in cell lines and xenograft mice models and has been associated with poor clinical prognosis in human cancers. Evidence accumulated in the last few years indicates that EMT-ATFs also regulate an expanding set of cancer cell capabilities beyond tumor invasion. Thus, EMT-ATFs have been shown to cooperate in oncogenic transformation, regulate cancer cell stemness, override safeguard programs against cancer like apoptosis and senescence, determine resistance to chemotherapy and promote tumor angiogenesis. This article reviews the expanding portfolio of functions played by EMT-ATFs in cancer progression.
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页码:3429 / 3456
页数:27
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