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Molecular Pharmacology

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Research ArticleArticle

Gene Transfer of Pro-opiomelanocortin Prohormone Suppressed the Growth and Metastasis of Melanoma: Involvement of α-Melanocyte-Stimulating Hormone-Mediated Inhibition of the Nuclear Factor κB/Cyclooxygenase-2 Pathway

Guei-Sheung Liu, Li-Fen Liu, Che-Jen Lin, Jui-Cheng Tseng, Ming-Ju Chuang, Hing-Chung Lam, Jenn-Kuen Lee, Lin-Cheng Yang, Julie Hwa Yu Chan, Shen-Long Howng and Ming-Hong Tai
Molecular Pharmacology February 2006, 69 (2) 440-451; DOI: https://doi.org/10.1124/mol.105.015404
Guei-Sheung Liu
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Li-Fen Liu
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Che-Jen Lin
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Jui-Cheng Tseng
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Ming-Ju Chuang
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Hing-Chung Lam
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Jenn-Kuen Lee
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Lin-Cheng Yang
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Julie Hwa Yu Chan
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Shen-Long Howng
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Ming-Hong Tai
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Abstract

Pro-opiomelanocortin (POMC) is a prohormone of various neuropeptides, including corticotropin, α-melanocyte-stimulating hormone (α-MSH), and β-endorphin (β-EP). POMC neuropeptides are potent inflammation inhibitors and immunosuppressants and may exert opposite influences during tumorigenesis. However, the role of POMC expression in carcinogenesis remains elusive. We evaluated the antineoplastic potential of POMC gene delivery in a syngenic B16-F10 melanoma model. Adenovirus-mediated POMC gene delivery in B16-F10 cells increased the release of POMC neuropeptides in cultured media, which differentially regulated the secretion of pro- and anti-inflammatory cytokines in lymphocytes. POMC gene transfer significantly reduced the anchorage-independent growth of melanoma cells. Moreover, pre- or post-treatment with POMC gene delivery effectively retarded the melanoma growth in mice. Intravenous injection of POMC-transduced B16-F10 cells resulted in reduced foci formation in lung by 60 to 70% of control. The reduced metastasis of POMC-transduced B16-F10 cells could be attributed to their attenuated migratory and adhesive capabilities. POMC gene delivery reduced the cyclooxygenase-2 (COX-2) expression and prostaglandin (PG) E2 synthesis in melanoma cells and tumor tissues. In addition, application of NS-398, a selective COX-2 inhibitor, mimicked the antineoplastic functions of POMC gene transfer in melanoma. The POMC-mediated COX-2 down-regulation was correlated with its inhibition of nuclear factor κB (NFκB) activities. Exogenous supply of α-MSH inhibited NFκB activities, whereas application of the α-MSH antagonist growth hormone-releasing peptide-6 (GHRP-6) abolished the POMC-induced inhibition of NFκB activities and melanoma growth in mice. In summary, POMC gene delivery suppresses melanoma via α-MSH-induced inhibition of NFκB/COX-2 pathway, thereby constituting a novel therapy for melanoma.

  • Received June 14, 2005.
  • Accepted November 2, 2005.
  • The American Society for Pharmacology and Experimental Therapeutics
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Molecular Pharmacology: 69 (2)
Molecular Pharmacology
Vol. 69, Issue 2
1 Feb 2006
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Gene Transfer of Pro-opiomelanocortin Prohormone Suppressed the Growth and Metastasis of Melanoma: Involvement of α-Melanocyte-Stimulating Hormone-Mediated Inhibition of the Nuclear Factor κB/Cyclooxygenase-2 Pathway
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Research ArticleArticle

Gene Transfer of Pro-opiomelanocortin Prohormone Suppressed the Growth and Metastasis of Melanoma: Involvement of α-Melanocyte-Stimulating Hormone-Mediated Inhibition of the Nuclear Factor κB/Cyclooxygenase-2 Pathway

Guei-Sheung Liu, Li-Fen Liu, Che-Jen Lin, Jui-Cheng Tseng, Ming-Ju Chuang, Hing-Chung Lam, Jenn-Kuen Lee, Lin-Cheng Yang, Julie Hwa Yu Chan, Shen-Long Howng and Ming-Hong Tai
Molecular Pharmacology February 1, 2006, 69 (2) 440-451; DOI: https://doi.org/10.1124/mol.105.015404

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Research ArticleArticle

Gene Transfer of Pro-opiomelanocortin Prohormone Suppressed the Growth and Metastasis of Melanoma: Involvement of α-Melanocyte-Stimulating Hormone-Mediated Inhibition of the Nuclear Factor κB/Cyclooxygenase-2 Pathway

Guei-Sheung Liu, Li-Fen Liu, Che-Jen Lin, Jui-Cheng Tseng, Ming-Ju Chuang, Hing-Chung Lam, Jenn-Kuen Lee, Lin-Cheng Yang, Julie Hwa Yu Chan, Shen-Long Howng and Ming-Hong Tai
Molecular Pharmacology February 1, 2006, 69 (2) 440-451; DOI: https://doi.org/10.1124/mol.105.015404
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