KISS1 metastasis suppression and emergent pathways

John F. Harms, Danny R. Welch, Mary E. Miele

Research output: Contribution to journalReview article

94 Citations (Scopus)

Abstract

Metastatic disease is the most critical impediment to cancer patient survival. However, comparatively little is known concerning the intricate pathways which govern the complex phenotypes associated with metastasis. The KISS1 metastasis suppressor gene inhibits metastasis in both in vivo melanoma and breast carcinoma models. Despite its clear physiological activity, the mechanism of KISS1 remains unclear. Recent identification of a 54 amino acid peptide of KISS1, termed metastin or kisspeptin-54, and its cognate G-protein coupled receptor (hOT7T175, AXOR12, GPR54) have provided additional clues and avenues of research. While studies have attributed KISS1 with modulation of NFκB regulation, experiments with metastin and its receptor implicate MAP kinase pathways and also suggest the potential of autocrine, paracrine and endocrine roles. Impacts on motility, chemotaxis, adhesion and invasion have each been documented in disparate cell lines and conflicting observations require resolution. Nevertheless, mounting clinical evidence, particularly the loss of KISS1 in metastases, correlates KISS1 and metastin receptor expression with human tumor progression. Together, the data substantiate roles for these molecules in metastasis regulation.

Original languageEnglish (US)
Pages (from-to)11-18
Number of pages8
JournalClinical and Experimental Metastasis
Volume20
Issue number1
DOIs
StatePublished - Mar 22 2003

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Kisspeptins
Neoplasm Metastasis
Chemotaxis
G-Protein-Coupled Receptors
Tumor Suppressor Genes
Melanoma
Neoplasms
Phosphotransferases
Breast Neoplasms
Phenotype
Amino Acids
Cell Line
Peptides
Survival
Research

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

Cite this

Harms, John F. ; Welch, Danny R. ; Miele, Mary E. / KISS1 metastasis suppression and emergent pathways. In: Clinical and Experimental Metastasis. 2003 ; Vol. 20, No. 1. pp. 11-18.
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KISS1 metastasis suppression and emergent pathways. / Harms, John F.; Welch, Danny R.; Miele, Mary E.

In: Clinical and Experimental Metastasis, Vol. 20, No. 1, 22.03.2003, p. 11-18.

Research output: Contribution to journalReview article

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AU - Harms, John F.

AU - Welch, Danny R.

AU - Miele, Mary E.

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N2 - Metastatic disease is the most critical impediment to cancer patient survival. However, comparatively little is known concerning the intricate pathways which govern the complex phenotypes associated with metastasis. The KISS1 metastasis suppressor gene inhibits metastasis in both in vivo melanoma and breast carcinoma models. Despite its clear physiological activity, the mechanism of KISS1 remains unclear. Recent identification of a 54 amino acid peptide of KISS1, termed metastin or kisspeptin-54, and its cognate G-protein coupled receptor (hOT7T175, AXOR12, GPR54) have provided additional clues and avenues of research. While studies have attributed KISS1 with modulation of NFκB regulation, experiments with metastin and its receptor implicate MAP kinase pathways and also suggest the potential of autocrine, paracrine and endocrine roles. Impacts on motility, chemotaxis, adhesion and invasion have each been documented in disparate cell lines and conflicting observations require resolution. Nevertheless, mounting clinical evidence, particularly the loss of KISS1 in metastases, correlates KISS1 and metastin receptor expression with human tumor progression. Together, the data substantiate roles for these molecules in metastasis regulation.

AB - Metastatic disease is the most critical impediment to cancer patient survival. However, comparatively little is known concerning the intricate pathways which govern the complex phenotypes associated with metastasis. The KISS1 metastasis suppressor gene inhibits metastasis in both in vivo melanoma and breast carcinoma models. Despite its clear physiological activity, the mechanism of KISS1 remains unclear. Recent identification of a 54 amino acid peptide of KISS1, termed metastin or kisspeptin-54, and its cognate G-protein coupled receptor (hOT7T175, AXOR12, GPR54) have provided additional clues and avenues of research. While studies have attributed KISS1 with modulation of NFκB regulation, experiments with metastin and its receptor implicate MAP kinase pathways and also suggest the potential of autocrine, paracrine and endocrine roles. Impacts on motility, chemotaxis, adhesion and invasion have each been documented in disparate cell lines and conflicting observations require resolution. Nevertheless, mounting clinical evidence, particularly the loss of KISS1 in metastases, correlates KISS1 and metastin receptor expression with human tumor progression. Together, the data substantiate roles for these molecules in metastasis regulation.

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