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Abstract Metastasis formation is an essential aspect of cancer, for which the molecular underpinning has long been subject to debate. Although the organ preference for dissemination is governed by tumor–host interactions on the epigenetic level there is a genetic basis to the ability of cancer cells to disseminate. Metastasis genes encode homing receptors, their ligands, and extracellular matrix-degrading proteinases, which jointly cause invasion and anchorage-independence. They are developmentally non-essential stress response genes that physiologically mediate the homing of immune system cells. Metastatic potential is conferred to cancer cells by aberrant expression or splicing of these genes. Oncogenes act upstream of metastasis genes. In cancer cells, oncogenic signaling activates distinct genetic programs leading to cell cycle progression and invasiveness, respectively. The expression of metastasis genes is regulated by multi-subunit transcription factor complexes. The identification of genes that direct cancer metastasis implicates them as candidate drug targets.
AbstractList Metastasis formation is an essential aspect of cancer, for which the molecular underpinning has long been subject to debate. Although the organ preference for dissemination is governed by tumor–host interactions on the epigenetic level there is a genetic basis to the ability of cancer cells to disseminate. Metastasis genes encode homing receptors, their ligands, and extracellular matrix-degrading proteinases, which jointly cause invasion and anchorage-independence. They are developmentally non-essential stress response genes that physiologically mediate the homing of immune system cells. Metastatic potential is conferred to cancer cells by aberrant expression or splicing of these genes. Oncogenes act upstream of metastasis genes. In cancer cells, oncogenic signaling activates distinct genetic programs leading to cell cycle progression and invasiveness, respectively. The expression of metastasis genes is regulated by multi-subunit transcription factor complexes. The identification of genes that direct cancer metastasis implicates them as candidate drug targets.
Metastasis formation is an essential aspect of cancer, for which the molecular underpinning has long been subject to debate. Although the organ preference for dissemination is governed by tumor-host interactions on the epigenetic level there is a genetic basis to the ability of cancer cells to disseminate. Metastasis genes encode homing receptors, their ligands, and extracellular matrix-degrading proteinases, which jointly cause invasion and anchorage-independence. They are developmentally non-essential stress response genes that physiologically mediate the homing of immune system cells. Metastatic potential is conferred to cancer cells by aberrant expression or splicing of these genes. Oncogenes act upstream of metastasis genes. In cancer cells, oncogenic signaling activates distinct genetic programs leading to cell cycle progression and invasiveness, respectively. The expression of metastasis genes is regulated by multi-subunit transcription factor complexes. The identification of genes that direct cancer metastasis implicates them as candidate drug targets.Metastasis formation is an essential aspect of cancer, for which the molecular underpinning has long been subject to debate. Although the organ preference for dissemination is governed by tumor-host interactions on the epigenetic level there is a genetic basis to the ability of cancer cells to disseminate. Metastasis genes encode homing receptors, their ligands, and extracellular matrix-degrading proteinases, which jointly cause invasion and anchorage-independence. They are developmentally non-essential stress response genes that physiologically mediate the homing of immune system cells. Metastatic potential is conferred to cancer cells by aberrant expression or splicing of these genes. Oncogenes act upstream of metastasis genes. In cancer cells, oncogenic signaling activates distinct genetic programs leading to cell cycle progression and invasiveness, respectively. The expression of metastasis genes is regulated by multi-subunit transcription factor complexes. The identification of genes that direct cancer metastasis implicates them as candidate drug targets.
Abstract Metastasis formation is an essential aspect of cancer, for which the molecular underpinning has long been subject to debate. Although the organ preference for dissemination is governed by tumor–host interactions on the epigenetic level there is a genetic basis to the ability of cancer cells to disseminate. Metastasis genes encode homing receptors, their ligands, and extracellular matrix-degrading proteinases, which jointly cause invasion and anchorage-independence. They are developmentally non-essential stress response genes that physiologically mediate the homing of immune system cells. Metastatic potential is conferred to cancer cells by aberrant expression or splicing of these genes. Oncogenes act upstream of metastasis genes. In cancer cells, oncogenic signaling activates distinct genetic programs leading to cell cycle progression and invasiveness, respectively. The expression of metastasis genes is regulated by multi-subunit transcription factor complexes. The identification of genes that direct cancer metastasis implicates them as candidate drug targets.
Author Weber, Georg F.
Author_xml – sequence: 1
  givenname: Georg F.
  surname: Weber
  fullname: Weber, Georg F.
  email: georg.weber@uc.edu
  organization: University of Cincinnati Academic Health Center, College of Pharmacy, 3225 Eden Avenue, Cincinnati, OH 45267-0004, USA
BackLink https://www.ncbi.nlm.nih.gov/pubmed/18522865$$D View this record in MEDLINE/PubMed
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Snippet Metastasis formation is an essential aspect of cancer, for which the molecular underpinning has long been subject to debate. Although the organ preference for...
Abstract Metastasis formation is an essential aspect of cancer, for which the molecular underpinning has long been subject to debate. Although the organ...
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SubjectTerms Anchorage-independence
Animals
Cancer
Cancer therapies
Cell Adhesion - genetics
Cell division
Cell Movement - genetics
Cell Proliferation
Gene amplification
Gene expression
Gene Expression Regulation, Neoplastic
Hematology, Oncology and Palliative Medicine
Humans
Hyaluronan Receptors - genetics
Hyaluronan Receptors - metabolism
Invasion
Kinases
Ligands
Metastasis
Mutation
Neoplasm Invasiveness
Neoplasm Metastasis - genetics
Neoplasms - genetics
Neoplasms - immunology
Neoplasms - metabolism
Neoplasms - pathology
Oncogene
Osteopontin - genetics
Osteopontin - metabolism
Oxidoreductases - metabolism
Phosphorylation
Protein Isoforms
Rodents
Signal transduction
Stress response
Transcription factors
Transcription, Genetic
Tumors
Title Molecular mechanisms of metastasis
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https://dx.doi.org/10.1016/j.canlet.2008.04.030
https://www.ncbi.nlm.nih.gov/pubmed/18522865
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