New insights into the role of ID proteins in breast cancer metastasis: a MET affair

The establishment of lethal metastases depends on the capacity of a small number of cancer cells to regenerate a tumor after entering a target organ. Stankic and colleagues have identified a role for the inhibitor of differentiation protein, ID1, as a critical regulator of breast cancer stem-like properties and metastatic colonization. Under the control of tumor growth factor-beta signaling, ID1 induces mesenchymal-epithelial transition at the metastatic site by antagonizing the activity of the basic helix-loop-helix transcription factor Twist1. This study sheds light on mechanisms that initiate metastatic outgrowth, and strengthens the concept that epithelial-mesenchymal plasticity is crucial at different stages of metastasis.

• Publication year

  2014

• Venue

  Breast Cancer Research

• Publication date

  2014-05-15

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1186/bcr3654PMID 25927844PMCID 4053215
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• c-Myc and Her2 cooperate to drive a stem-like phenotype with poor prognosis in breast cancer

  2014cited by this paper
• New insights into the role of ID proteins in breast cancer metastasis: a MET affair

  2014cited by this paper
• The ID proteins: master regulators of cancer stem cells and tumour aggressiveness

  2014cited by this paper
• TGF-β-Id1 signaling opposes Twist1 and promotes metastatic colonization via a mesenchymal-to-epithelial transition.

  2013cited by this paper
• The roles of TGFβ in the tumour microenvironment

  2013cited by this paper
• Epithelial-mesenchymal transition can suppress major attributes of human epithelial tumor-initiating cells.

  2012cited by this paper
• To differentiate or not — routes towards metastasis

  2012cited by this paper
• Epithelial-mesenchymal transitions in development and disease.

  2009cited by this paper
• Id1 cooperates with oncogenic Ras to induce metastatic mammary carcinoma by subversion of the cellular senescence response

  2008cited by this paper
• Generation of Breast Cancer Stem Cells through Epithelial-Mesenchymal Transition

  2008cited by this paper
• The epithelial-mesenchymal transition generates cells with properties of stem cells.

  2008cited by this paper
• ID genes mediate tumor reinitiation during breast cancer lung metastasis

  2007cited by this paper
• Genes that mediate breast cancer metastasis to lung

  2005cited by this paper
• Overexpression of Id‐1 is associated with poor clinical outcome in node negative breast cancer

  2003cited by this paper

• Epigenetic Mechanisms in Neuroendocrine Neoplasms: Is There a Place for Inhibitors of DNA Binding Proteins?

  2025cites this paper
• Microarray Analysis of the Transcriptome of Peripheral Blood Lymphocytes in Breast Cancer Patients

  2025cites this paper
• Functional Enrichment Analysis of Tumor Microenvironment–Driven Molecular Alterations That Facilitate Epithelial-to-Mesenchymal Transition and Distant Metastasis

  2024cites this paper
• Inhibitor of Differentiation 1 (Id1) in Cancer and Cancer Therapy

  2020cites this paper
• Similarities Between Embryo Development and Cancer Process Suggest New Strategies for Research and Therapy of Tumors: A New Point of View

  2019cites this paper
• Targeting of a Helix‐Loop‐Helix Transcriptional Regulator by a Short Helical Peptide

  2017cites this paper
• Ring finger protein 125, as a potential highly aggressive and unfavorable prognostic biomarker, promotes the invasion and metastasis of human gallbladder cancers via activating the TGF-β1-SMAD3-ID1 signaling pathway

  2017cites this paper
• The Id-protein family in developmental and cancer-associated pathways

  2017cites this paper