A melanin‐independent interaction between Mc1r and Met signaling pathways is required for HGF‐dependent melanoma
Melanocortin 1 receptor (MC1R) signaling stimulates black eumelanin production through a cAMP‐dependent pathway. MC1R polymorphisms can impair this process, resulting in a predominance of red phaeomelanin. The red hair, fair skin and UV sensitive phenotype is a well‐described melanoma risk factor. M...
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| Published in | International journal of cancer Vol. 136; no. 4; pp. 752 - 760 |
|---|---|
| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Wiley Subscription Services, Inc
15.02.2015
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0020-7136 1097-0215 1097-0215 |
| DOI | 10.1002/ijc.29050 |
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| Abstract | Melanocortin 1 receptor (MC1R) signaling stimulates black eumelanin production through a cAMP‐dependent pathway. MC1R polymorphisms can impair this process, resulting in a predominance of red phaeomelanin. The red hair, fair skin and UV sensitive phenotype is a well‐described melanoma risk factor. MC1R polymorphisms also confer melanoma risk independent of pigment. We investigated the effect of Mc1r deficiency in a mouse model of UV‐induced melanoma. C57BL/6‐Mc1r+/+‐HGF transgenic mice have a characteristic hyperpigmented black phenotype with extra‐follicular dermal melanocytes located at the dermal/epidermal junction. UVB induces melanoma, independent of melanin pigmentation, but UVA‐induced and spontaneous melanomas are dependent on black eumelanin. We crossed these mice with yellow C57BL/6‐Mc1re/e animals which have a non‐functional Mc1r and produce predominantly yellow phaeomelanin. Yellow C57BL/6‐Mc1re/e‐HGF mice produced no melanoma in response to UVR or spontaneously even though the HGF transgene and its receptor Met were expressed. Total melanin was less than in C57BL/6‐Mc1r+/+‐HGF mice, hyperpigmentation was not observed and there were few extra‐follicular melanocytes. Thus, functional Mc1r was required for expression of the transgenic HGF phenotype. Heterozygous C57BL/6‐Mc1re/+‐HGF mice were black and hyperpigmented and, although extra‐follicular melanocytes and skin melanin content were similar to C57BL/6‐Mc1r+/+‐HGF animals, they developed UV‐induced and spontaneous melanomas with significantly less efficiency by all criteria. Thus, heterozygosity for Mc1r was sufficient to restore the transgenic HGF phenotype but insufficient to fully restore melanoma. We conclude that a previously unsuspected melanin‐independent interaction between Mc1r and Met signaling pathways is required for HGF‐dependent melanoma and postulate that this pathway is involved in human melanoma.
What's new?
Melanocortin 1 receptor (MC1R), which plays a central role in the production of melanin, is subject to marked genetic variation, with certain variants increasing melanoma risk through fair skin phenotype. Others MCR1 variants, however, influence melanoma risk through pigment‐independent alterations. Such variants may include those that affect interactions between Mc1r and hepatocyte growth factor (HGF)/Met signaling, as suggested by this investigation of Mcr1 deficiency in a UV‐induced melanoma mouse model. HGF has been implicated in tumor escape from B‐RAF inhibitors in human melanoma, and MET is a target for melanoma therapy, suggesting potential therapeutic significance for the findings. |
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| AbstractList | Melanocortin 1 receptor (MC1R) signaling stimulates black eumelanin production through a cAMP-dependent pathway. MC1R polymorphisms can impair this process, resulting in a predominance of red phaeomelanin. The red hair, fair skin and UV sensitive phenotype is a well-described melanoma risk factor. MC1R polymorphisms also confer melanoma risk independent of pigment. We investigated the effect of Mc1r deficiency in a mouse model of UV-induced melanoma. C57BL/6-Mc1r+/+-HGF transgenic mice have a characteristic hyperpigmented black phenotype with extra-follicular dermal melanocytes located at the dermal/epidermal junction. UVB induces melanoma, independent of melanin pigmentation, but UVA-induced and spontaneous melanomas are dependent on black eumelanin. We crossed these mice with yellow C57BL/6-Mc1re/e animals which have a non-functional Mc1r and produce predominantly yellow phaeomelanin. Yellow C57BL/6-Mc1re/e-HGF mice produced no melanoma in response to UVR or spontaneously even though the HGF transgene and its receptor Met were expressed. Total melanin was less than in C57BL/6-Mc1r+/+-HGF mice, hyperpigmentation was not observed and there were few extra-follicular melanocytes. Thus, functional Mc1r was required for expression of the transgenic HGF phenotype. Heterozygous C57BL/6-Mc1re/+-HGF mice were black and hyperpigmented and, although extra-follicular melanocytes and skin melanin content were similar to C57BL/6-Mc1r+/+-HGF animals, they developed UV-induced and spontaneous melanomas with significantly less efficiency by all criteria. Thus, heterozygosity for Mc1r was sufficient to restore the transgenic HGF phenotype but insufficient to fully restore melanoma. We conclude that a previously unsuspected melanin-independent interaction between Mc1r and Met signaling pathways is required for HGF-dependent melanoma and postulate that this pathway is involved in human melanoma. What's new? Melanocortin 1 receptor (MC1R), which plays a central role in the production of melanin, is subject to marked genetic variation, with certain variants increasing melanoma risk through fair skin phenotype. Others MCR1 variants, however, influence melanoma risk through pigment-independent alterations. Such variants may include those that affect interactions between Mc1r and hepatocyte growth factor (HGF)/Met signaling, as suggested by this investigation of Mcr1 deficiency in a UV-induced melanoma mouse model. HGF has been implicated in tumor escape from B-RAF inhibitors in human melanoma, and MET is a target for melanoma therapy, suggesting potential therapeutic significance for the findings. Melanocortin 1 receptor (MC1R) signaling stimulates black eumelanin production through a cAMP-dependent pathway. MC1R polymorphisms can impair this process, resulting in a predominance of red phaeomelanin. The red hair, fair skin and UV sensitive phenotype is a well-described melanoma risk factor. MC1R polymorphisms also confer melanoma risk independent of pigment. We investigated the effect of Mc1r deficiency in a mouse model of UV-induced melanoma. C57BL/6-Mc1r+/+-HGF transgenic mice have a characteristic hyperpigmented black phenotype with extra-follicular dermal melanocytes located at the dermal/epidermal junction. UVB induces melanoma, independent of melanin pigmentation, but UVA-induced and spontaneous melanomas are dependent on black eumelanin. We crossed these mice with yellow C57BL/6-Mc1re/e animals which have a non-functional Mc1r and produce predominantly yellow phaeomelanin. Yellow C57BL/6-Mc1re/e-HGF mice produced no melanoma in response to UVR or spontaneously even though the HGF transgene and its receptor Met were expressed. Total melanin was less than in C57BL/6-Mc1r+/+-HGF mice, hyperpigmentation was not observed and there were few extra-follicular melanocytes. Thus, functional Mc1r was required for expression of the transgenic HGF phenotype. Heterozygous C57BL/6-Mc1re/+-HGF mice were black and hyperpigmented and, although extra-follicular melanocytes and skin melanin content were similar to C57BL/6-Mc1r+/+-HGF animals, they developed UV-induced and spontaneous melanomas with significantly less efficiency by all criteria. Thus, heterozygosity for Mc1r was sufficient to restore the transgenic HGF phenotype but insufficient to fully restore melanoma. We conclude that a previously unsuspected melanin-independent interaction between Mc1r and Met signaling pathways is required for HGF-dependent melanoma and postulate that this pathway is involved in human melanoma. Melanocortin 1 receptor (MC1R) signaling stimulates black eumelanin production through a cAMP‐dependent pathway. MC1R polymorphisms can impair this process, resulting in a predominance of red phaeomelanin. The red hair, fair skin and UV sensitive phenotype is a well‐described melanoma risk factor. MC1R polymorphisms also confer melanoma risk independent of pigment. We investigated the effect of Mc1r deficiency in a mouse model of UV‐induced melanoma. C57BL/6‐Mc1r+/+‐HGF transgenic mice have a characteristic hyperpigmented black phenotype with extra‐follicular dermal melanocytes located at the dermal/epidermal junction. UVB induces melanoma, independent of melanin pigmentation, but UVA‐induced and spontaneous melanomas are dependent on black eumelanin. We crossed these mice with yellow C57BL/6‐Mc1re/e animals which have a non‐functional Mc1r and produce predominantly yellow phaeomelanin. Yellow C57BL/6‐Mc1re/e‐HGF mice produced no melanoma in response to UVR or spontaneously even though the HGF transgene and its receptor Met were expressed. Total melanin was less than in C57BL/6‐Mc1r+/+‐HGF mice, hyperpigmentation was not observed and there were few extra‐follicular melanocytes. Thus, functional Mc1r was required for expression of the transgenic HGF phenotype. Heterozygous C57BL/6‐Mc1re/+‐HGF mice were black and hyperpigmented and, although extra‐follicular melanocytes and skin melanin content were similar to C57BL/6‐Mc1r+/+‐HGF animals, they developed UV‐induced and spontaneous melanomas with significantly less efficiency by all criteria. Thus, heterozygosity for Mc1r was sufficient to restore the transgenic HGF phenotype but insufficient to fully restore melanoma. We conclude that a previously unsuspected melanin‐independent interaction between Mc1r and Met signaling pathways is required for HGF‐dependent melanoma and postulate that this pathway is involved in human melanoma. What's new? Melanocortin 1 receptor (MC1R), which plays a central role in the production of melanin, is subject to marked genetic variation, with certain variants increasing melanoma risk through fair skin phenotype. Others MCR1 variants, however, influence melanoma risk through pigment‐independent alterations. Such variants may include those that affect interactions between Mc1r and hepatocyte growth factor (HGF)/Met signaling, as suggested by this investigation of Mcr1 deficiency in a UV‐induced melanoma mouse model. HGF has been implicated in tumor escape from B‐RAF inhibitors in human melanoma, and MET is a target for melanoma therapy, suggesting potential therapeutic significance for the findings. Melanocortin 1 receptor (MC1R) signaling stimulates black eumelanin production through a cAMP-dependent pathway. MC1R polymorphisms can impair this process, resulting in a predominance of red phaeomelanin. The red hair, fair skin and UV sensitive phenotype is a well-described melanoma risk factor. MC1R polymorphisms also confer melanoma risk independent of pigment. We investigated the effect of Mc1r deficiency in a mouse model of UV-induced melanoma. C57BL/6-Mc1r+/+-HGF transgenic mice have a characteristic hyperpigmented black phenotype with extra-follicular dermal melanocytes located at the dermal/epidermal junction. UVB induces melanoma, independent of melanin pigmentation, but UVA-induced and spontaneous melanomas are dependent on black eumelanin. We crossed these mice with yellow C57BL/6-Mc1re/e animals which have a non-functional Mc1r and produce predominantly yellow phaeomelanin. Yellow C57BL/6-Mc1re/e-HGF mice produced no melanoma in response to UVR or spontaneously even though the HGF transgene and its receptor Met were expressed. Total melanin was less than in C57BL/6-Mc1r+/+-HGF mice, hyperpigmentation was not observed and there were few extra-follicular melanocytes. Thus, functional Mc1r was required for expression of the transgenic HGF phenotype. Heterozygous C57BL/6-Mc1re/+-HGF mice were black and hyperpigmented and, although extra-follicular melanocytes and skin melanin content were similar to C57BL/6-Mc1r+/+-HGF animals, they developed UV-induced and spontaneous melanomas with significantly less efficiency by all criteria. Thus, heterozygosity for Mc1r was sufficient to restore the transgenic HGF phenotype but insufficient to fully restore melanoma. We conclude that a previously unsuspected melanin-independent interaction between Mc1r and Met signaling pathways is required for HGF-dependent melanoma and postulate that this pathway is involved in human melanoma.Melanocortin 1 receptor (MC1R) signaling stimulates black eumelanin production through a cAMP-dependent pathway. MC1R polymorphisms can impair this process, resulting in a predominance of red phaeomelanin. The red hair, fair skin and UV sensitive phenotype is a well-described melanoma risk factor. MC1R polymorphisms also confer melanoma risk independent of pigment. We investigated the effect of Mc1r deficiency in a mouse model of UV-induced melanoma. C57BL/6-Mc1r+/+-HGF transgenic mice have a characteristic hyperpigmented black phenotype with extra-follicular dermal melanocytes located at the dermal/epidermal junction. UVB induces melanoma, independent of melanin pigmentation, but UVA-induced and spontaneous melanomas are dependent on black eumelanin. We crossed these mice with yellow C57BL/6-Mc1re/e animals which have a non-functional Mc1r and produce predominantly yellow phaeomelanin. Yellow C57BL/6-Mc1re/e-HGF mice produced no melanoma in response to UVR or spontaneously even though the HGF transgene and its receptor Met were expressed. Total melanin was less than in C57BL/6-Mc1r+/+-HGF mice, hyperpigmentation was not observed and there were few extra-follicular melanocytes. Thus, functional Mc1r was required for expression of the transgenic HGF phenotype. Heterozygous C57BL/6-Mc1re/+-HGF mice were black and hyperpigmented and, although extra-follicular melanocytes and skin melanin content were similar to C57BL/6-Mc1r+/+-HGF animals, they developed UV-induced and spontaneous melanomas with significantly less efficiency by all criteria. Thus, heterozygosity for Mc1r was sufficient to restore the transgenic HGF phenotype but insufficient to fully restore melanoma. We conclude that a previously unsuspected melanin-independent interaction between Mc1r and Met signaling pathways is required for HGF-dependent melanoma and postulate that this pathway is involved in human melanoma. Melanocortin 1 receptor (MC1R) signaling stimulates black eumelanin production through a cAMP dependent pathway. MC1R polymorphisms can impair this process, resulting in a predominance of red phaeomelanin. The red hair, fair skin and UV sensitive phenotype is a well-described melanoma risk factor. MC1R polymorphisms also confer melanoma risk independent of pigment. We investigated the effect of Mc1r deficiency in a mouse model of UV-induced melanoma. C57BL/6-Mc1r +/+ -HGF transgenic mice have a characteristic hyperpigmented black phenotype with extra-follicular dermal melanocytes located at the dermal/epidermal junction. UVB induces melanoma, independent of melanin pigmentation, but UVA-induced and spontaneous melanomas are dependent on black eumelanin. We crossed these mice with yellow C57BL/6-Mc1r e/e animals which have a non-functional Mc1r and produce predominantly yellow phaeomelanin. Yellow C57BL/6-Mc1r e/e -HGF mice produced no melanoma in response to UVR or spontaneously even though the HGF transgene and its receptor Met were expressed. Total melanin was less than in C57BL/6-Mc1r +/+ -HGF mice, hyperpigmentation was not observed and there were few extra-follicular melanocytes. Thus, functional Mc1r was required for expression of the transgenic HGF phenotype. Heterozygous C57BL/6-Mc1r e/+ -HGF mice were black and hyperpigmented and, although extra-follicular melanocytes and skin melanin content were similar to C57BL/6-Mc1r +/+ -HGF animals, they developed UV-induced and spontaneous melanomas with significantly less efficiency by all criteria. Thus, heterozygosity for Mc1r was sufficient to restore the transgenic HGF phenotype but insufficient to fully restore melanoma. We conclude that a previously unsuspected melanin-independent interaction between Mc1r and Met signaling pathways is required for HGF-dependent melanoma and postulate that this pathway is involved in human melanoma. Melanocortin 1 receptor (MC1R) signaling stimulates black eumelanin production through a cAMP‐dependent pathway. MC1R polymorphisms can impair this process, resulting in a predominance of red phaeomelanin. The red hair, fair skin and UV sensitive phenotype is a well‐described melanoma risk factor. MC1R polymorphisms also confer melanoma risk independent of pigment. We investigated the effect of Mc1r deficiency in a mouse model of UV‐induced melanoma. C57BL/6‐Mc1r +/+ ‐HGF transgenic mice have a characteristic hyperpigmented black phenotype with extra‐follicular dermal melanocytes located at the dermal/epidermal junction. UVB induces melanoma, independent of melanin pigmentation, but UVA‐induced and spontaneous melanomas are dependent on black eumelanin. We crossed these mice with yellow C57BL/6‐Mc1r e/e animals which have a non‐functional Mc1r and produce predominantly yellow phaeomelanin. Yellow C57BL/6‐Mc1r e/e ‐HGF mice produced no melanoma in response to UVR or spontaneously even though the HGF transgene and its receptor Met were expressed. Total melanin was less than in C57BL/6‐Mc1r +/+ ‐HGF mice, hyperpigmentation was not observed and there were few extra‐follicular melanocytes. Thus, functional Mc1r was required for expression of the transgenic HGF phenotype. Heterozygous C57BL/6‐Mc1r e/+ ‐HGF mice were black and hyperpigmented and, although extra‐follicular melanocytes and skin melanin content were similar to C57BL/6‐Mc1r +/+ ‐HGF animals, they developed UV‐induced and spontaneous melanomas with significantly less efficiency by all criteria. Thus, heterozygosity for Mc1r was sufficient to restore the transgenic HGF phenotype but insufficient to fully restore melanoma. We conclude that a previously unsuspected melanin‐independent interaction between Mc1r and Met signaling pathways is required for HGF‐dependent melanoma and postulate that this pathway is involved in human melanoma. What's new? Melanocortin 1 receptor (MC1R), which plays a central role in the production of melanin, is subject to marked genetic variation, with certain variants increasing melanoma risk through fair skin phenotype. Others MCR1 variants, however, influence melanoma risk through pigment‐independent alterations. Such variants may include those that affect interactions between Mc1r and hepatocyte growth factor (HGF)/Met signaling, as suggested by this investigation of Mcr1 deficiency in a UV‐induced melanoma mouse model. HGF has been implicated in tumor escape from B‐RAF inhibitors in human melanoma, and MET is a target for melanoma therapy, suggesting potential therapeutic significance for the findings. |
| Author | Noonan, Frances P. Strickland, Faith M. Wielgus, Albert Merlino, Glenn Fabo, Edward C. Wolnicka‐Glubisz, Agnieszka Anver, Miriam |
| AuthorAffiliation | 2 Jagiellonian University, Faculty of Biochemistry, Biophysics and Biotechnology, Department of Biophysics, Krakow, Poland 4 Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, North Carolina 27709, USA 1 Department of Microbiology, Immunology and Tropical Medicine, The George Washington University, Washington DC 20037, USA 3 Department of Dermatology, The Henry Ford Health Sciences Center, One Ford Place, Detroit, MI 48202, USA 5 Pathology/Histotechnology Laboratory Frederick National Laboratory for Cancer Research, Frederick MD 21702, USA 6 Laboratory of Cancer Biology & Genetics, National Cancer Institute, NIH, Bethesda MD 20892, USA |
| AuthorAffiliation_xml | – name: 4 Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, North Carolina 27709, USA – name: 5 Pathology/Histotechnology Laboratory Frederick National Laboratory for Cancer Research, Frederick MD 21702, USA – name: 1 Department of Microbiology, Immunology and Tropical Medicine, The George Washington University, Washington DC 20037, USA – name: 2 Jagiellonian University, Faculty of Biochemistry, Biophysics and Biotechnology, Department of Biophysics, Krakow, Poland – name: 3 Department of Dermatology, The Henry Ford Health Sciences Center, One Ford Place, Detroit, MI 48202, USA – name: 6 Laboratory of Cancer Biology & Genetics, National Cancer Institute, NIH, Bethesda MD 20892, USA |
| Author_xml | – sequence: 1 givenname: Agnieszka surname: Wolnicka‐Glubisz fullname: Wolnicka‐Glubisz, Agnieszka organization: Biophysics and Biotechnology, Jagiellonian University – sequence: 2 givenname: Faith M. surname: Strickland fullname: Strickland, Faith M. organization: The Henry Ford Health Sciences Center – sequence: 3 givenname: Albert surname: Wielgus fullname: Wielgus, Albert organization: National Institute of Environmental Health Sciences, NIH – sequence: 4 givenname: Miriam surname: Anver fullname: Anver, Miriam organization: Pathology/Histotechnology Laboratory Frederick National Laboratory for Cancer Research – sequence: 5 givenname: Glenn surname: Merlino fullname: Merlino, Glenn organization: National Cancer Institute, NIH – sequence: 6 givenname: Edward C. surname: Fabo fullname: Fabo, Edward C. organization: Immunology and Tropical Medicine, The George Washington University – sequence: 7 givenname: Frances P. surname: Noonan fullname: Noonan, Frances P. organization: Immunology and Tropical Medicine, The George Washington University |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24975581$$D View this record in MEDLINE/PubMed |
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| Keywords | melanocortin 1 receptor melanoma HGF/Met melanin ultraviolet |
| Language | English |
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| Notes | Faith M. Strickland's current address is: Department of Internal Medicine, Rheumatology Division, The University of Michigan, Ann Arbor, MI 48109‐2200 Published 2014. This article is a US Government work and, as such, is in the public domain of the United States of America. Albert Wielgus's current address is: Lineberger Comprehensive Cancer Center, 160 N. Medical Dr., University of North Carolina, Chapel Hill, NC 27599, USA ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Current Address: Lineberger Comprehensive Cancer Center, 160 N. Medical Dr., University of North Carolina, Chapel Hill, NC 27599, USA Current Address: Department of Internal Medicine, Rheumatology Division, The University of Michigan, Ann Arbor, MI 48109-2200 |
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| Snippet | Melanocortin 1 receptor (MC1R) signaling stimulates black eumelanin production through a cAMP‐dependent pathway. MC1R polymorphisms can impair this process,... Melanocortin 1 receptor (MC1R) signaling stimulates black eumelanin production through a cAMP-dependent pathway. MC1R polymorphisms can impair this process,... Melanocortin 1 receptor (MC1R) signaling stimulates black eumelanin production through a cAMP dependent pathway. MC1R polymorphisms can impair this process,... |
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| SubjectTerms | Animals Cancer Female Genotype & phenotype Hepatocyte Growth Factor - physiology HGF/Met Humans Male Medical research melanin Melanins - physiology melanocortin 1 receptor Melanoma Melanoma, Experimental - metabolism Melanoma, Experimental - pathology Mice, Inbred C57BL Mice, Transgenic Proto-Oncogene Proteins c-met - metabolism Receptor, Melanocortin, Type 1 - metabolism Rodents Signal Transduction Skin Neoplasms - metabolism Skin Neoplasms - pathology ultraviolet |
| Title | A melanin‐independent interaction between Mc1r and Met signaling pathways is required for HGF‐dependent melanoma |
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