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Title:
EMT, cell plasticity and metastasis | Cancer and Metastasis Reviews
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Carcinoma cells that are induced to suppress their epithelial features and upregulate mesenchymal gene expression programs acquire traits that promote an invasive and metastatic phenotype. This is achieved through the expression of a program termed the epithelial-to-mesenchymal transition (EMT)—a fundamental cell-biological process that plays key roles in embryogenesis and wound healing. Re-activation of the EMT during cancer promotes disease progression and enhances the metastatic phenotype by bestowing upon previously benign carcinoma cell traits such as migration, invasion, resistance to anoikis, chemoresistance and tumour-initiating potential. Herein, we discuss recent insights into the function of the EMT and cancer cell plasticity during cancer progression, with a focus on their role in promoting successful completion of the later stages of the metastatic cascade.
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pubmed, article, google, scholar, cancer, cas, cell, central, cells, transition, metastasis, research, epithelialmesenchymal, breast, nature, emt, biology, stem, plasticity, chaffer, weinberg, journal, progression, tumor, reviews, metastatic, states, privacy, cookies, content, lim, robert, carcinoma, phenotype, epithelialtomesenchymal, promotes, role, molecular, publish, search, elgene, abstract, epithelial, mesenchymal, expression, resistance, access, mechanisms, therapy, signaling,
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- Snail, Zeb and bHLH factors in tumour progression: an alliance against the epithelial phenotype?
- The ZEB/miR-200 feedback loop--a motor of cellular plasticity in development and cancer?
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headline:EMT, cell plasticity and metastasis
description:Carcinoma cells that are induced to suppress their epithelial features and upregulate mesenchymal gene expression programs acquire traits that promote an invasive and metastatic phenotype. This is achieved through the expression of a program termed the epithelial-to-mesenchymal transition (EMT)—a fundamental cell-biological process that plays key roles in embryogenesis and wound healing. Re-activation of the EMT during cancer promotes disease progression and enhances the metastatic phenotype by bestowing upon previously benign carcinoma cell traits such as migration, invasion, resistance to anoikis, chemoresistance and tumour-initiating potential. Herein, we discuss recent insights into the function of the EMT and cancer cell plasticity during cancer progression, with a focus on their role in promoting successful completion of the later stages of the metastatic cascade.
datePublished:2016-11-22T00:00:00Z
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EMT
Cancer cell plasticity
Metastasis
Partial-EMT
Tumor-initiating cells (TICs)
Cancer Research
Oncology
Biomedicine
general
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headline:EMT, cell plasticity and metastasis
description:Carcinoma cells that are induced to suppress their epithelial features and upregulate mesenchymal gene expression programs acquire traits that promote an invasive and metastatic phenotype. This is achieved through the expression of a program termed the epithelial-to-mesenchymal transition (EMT)—a fundamental cell-biological process that plays key roles in embryogenesis and wound healing. Re-activation of the EMT during cancer promotes disease progression and enhances the metastatic phenotype by bestowing upon previously benign carcinoma cell traits such as migration, invasion, resistance to anoikis, chemoresistance and tumour-initiating potential. Herein, we discuss recent insights into the function of the EMT and cancer cell plasticity during cancer progression, with a focus on their role in promoting successful completion of the later stages of the metastatic cascade.
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EMT
Cancer cell plasticity
Metastasis
Partial-EMT
Tumor-initiating cells (TICs)
Cancer Research
Oncology
Biomedicine
general
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