Protein kinase Cε, which sensitizes skin to sun's UV radiation-induced cutaneous damage and development of squamous cell carcinomas, associates with stat3
Chronic exposure to UV radiation (UVR) is the major etiologic factor in the development of human skin cancers including squamous cell carcinoma (SCC). We have shown that protein kinase C(epsilon) (PKC(epsilon)), a Ca(2+)-independent, phospholipid-dependent serine/threonine kinase, is an endogenous p...
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Published in | Cancer research (Chicago, Ill.) Vol. 67; no. 3; pp. 1385 - 1394 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
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Philadelphia, PA
American Association for Cancer Research
01.02.2007
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Abstract | Chronic exposure to UV radiation (UVR) is the major etiologic factor in the development of human skin cancers including squamous cell carcinoma (SCC). We have shown that protein kinase C(epsilon) (PKC(epsilon)), a Ca(2+)-independent, phospholipid-dependent serine/threonine kinase, is an endogenous photosensitizer. PKC(epsilon) is among the six isoforms (alpha, delta, epsilon, eta, mu, and zeta) expressed in both mouse and human skin. PKC(epsilon) transgenic mice, which overexpress PKC(epsilon) in the basal epidermal cells and cells of the hair follicle, are highly sensitive to UVR-induced cutaneous damage and development of SCC. We now present that PKC(epsilon)-overexpressing, but not PKC(delta)-overexpressing, transgenic mice, when exposed to a single (4 kJ/m(2)) or repeated (four doses, 2 kJ/m(2)/dose, thrice weekly) UVR, emitted by Kodacel-filtered FS-40 sun lamps, elicit constitutive phosphorylation of signal transducers and activators of transcription 3 (Stat3) at both Tyr705 and Ser727 residues. UVR-induced phosphorylation of Stat3 accompanied increased expression of Stat3-regulated genes (c-myc, cyclin D1, cdc25A, and COX-2). In reciprocal immunoprecipitation/blotting experiments, phosphorylated Stat3 co-immunoprecipitated with PKC(epsilon). As observed in vivo using PKC(epsilon) knockout mice and in vitro in an immunocomplex kinase assay, PKC(epsilon) phosphorylated Stat3 at Ser727 residue. These results indicate for the first time that (a) PKC(epsilon) is a Stat3Ser727 kinase; (b) PKC(epsilon)-mediated phosphorylation of StatSer727 may be essential for transcriptional activity of Stat3; and (c) UVR-induced phosphorylation of Ser727 may be a key component of the mechanism by which PKC(epsilon) imparts sensitivity to UVR-induced development of SCC. |
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AbstractList | Chronic exposure to UV radiation (UVR) is the major etiologic factor in the development of human skin cancers including squamous cell carcinoma (SCC). We have shown that protein kinase C(epsilon) (PKC(epsilon)), a Ca(2+)-independent, phospholipid-dependent serine/threonine kinase, is an endogenous photosensitizer. PKC(epsilon) is among the six isoforms (alpha, delta, epsilon, eta, mu, and zeta) expressed in both mouse and human skin. PKC(epsilon) transgenic mice, which overexpress PKC(epsilon) in the basal epidermal cells and cells of the hair follicle, are highly sensitive to UVR-induced cutaneous damage and development of SCC. We now present that PKC(epsilon)-overexpressing, but not PKC(delta)-overexpressing, transgenic mice, when exposed to a single (4 kJ/m(2)) or repeated (four doses, 2 kJ/m(2)/dose, thrice weekly) UVR, emitted by Kodacel-filtered FS-40 sun lamps, elicit constitutive phosphorylation of signal transducers and activators of transcription 3 (Stat3) at both Tyr705 and Ser727 residues. UVR-induced phosphorylation of Stat3 accompanied increased expression of Stat3-regulated genes (c-myc, cyclin D1, cdc25A, and COX-2). In reciprocal immunoprecipitation/blotting experiments, phosphorylated Stat3 co-immunoprecipitated with PKC(epsilon). As observed in vivo using PKC(epsilon) knockout mice and in vitro in an immunocomplex kinase assay, PKC(epsilon) phosphorylated Stat3 at Ser727 residue. These results indicate for the first time that (a) PKC(epsilon) is a Stat3Ser727 kinase; (b) PKC(epsilon)-mediated phosphorylation of StatSer727 may be essential for transcriptional activity of Stat3; and (c) UVR-induced phosphorylation of Ser727 may be a key component of the mechanism by which PKC(epsilon) imparts sensitivity to UVR-induced development of SCC. Chronic exposure to UV radiation (UVR) is the major etiologic factor in the development of human skin cancers including squamous cell carcinoma (SCC). We have shown that protein kinase C epsilon (PKC epsilon ), a Ca super(2+)-independent, phospholipid-dependent serine/threonine kinase, is an endogenous photosensitizer. PKC epsilon is among the six isoforms ( alpha , delta , epsilon , eta , mu , and zeta ) expressed in both mouse and human skin. PKC epsilon transgenic mice, which overexpress PKC epsilon in the basal epidermal cells and cells of the hair follicle, are highly sensitive to UVR-induced cutaneous damage and development of SCC. We now present that PKC epsilon -overexpressing, but not PKC delta -overexpressing, transgenic mice, when exposed to a single (4 kJ/m super(2)) or repeated (four doses, 2 kJ/m super(2)/dose, thrice weekly) UVR, emitted by Kodacel-filtered FS-40 sun lamps, elicit constitutive phosphorylation of signal transducers and activators of transcription 3 (Stat3) at both Tyr705 and Ser727 residues. UVR-induced phosphorylation of Stat3 accompanied increased expression of Stat3-regulated genes (c-myc, cyclin D1, cdc25A, and COX-2). In reciprocal immunoprecipitation/blotting experiments, phosphorylated Stat3 coimmunoprecipitated with PKC epsilon . As observed in vivo using PKC epsilon knockout mice and in vitro in an immunocomplex kinase assay, PKC epsilon phosphorylated Stat3 at Ser727 residue. These results indicate for the first time that (a) PKC epsilon is a Stat3Ser727 kinase; (b) PKC epsilon -mediated phosphorylation of StatSer727 may be essential for transcriptional activity of Stat3; and (c) UVR-induced phosphorylation of Ser727 may be a key component of the mechanism by which PKC epsilon imparts sensitivity to UVR-induced development of SCC. [Cancer Res 2007; 67(3):1385-94] Abstract Chronic exposure to UV radiation (UVR) is the major etiologic factor in the development of human skin cancers including squamous cell carcinoma (SCC). We have shown that protein kinase Cε (PKCε), a Ca2+-independent, phospholipid-dependent serine/threonine kinase, is an endogenous photosensitizer. PKCε is among the six isoforms (α, δ, ε, η, μ, and ζ) expressed in both mouse and human skin. PKCε transgenic mice, which overexpress PKCε in the basal epidermal cells and cells of the hair follicle, are highly sensitive to UVR-induced cutaneous damage and development of SCC. We now present that PKCε-overexpressing, but not PKCδ-overexpressing, transgenic mice, when exposed to a single (4 kJ/m2) or repeated (four doses, 2 kJ/m2/dose, thrice weekly) UVR, emitted by Kodacel-filtered FS-40 sun lamps, elicit constitutive phosphorylation of signal transducers and activators of transcription 3 (Stat3) at both Tyr705 and Ser727 residues. UVR-induced phosphorylation of Stat3 accompanied increased expression of Stat3-regulated genes (c-myc, cyclin D1, cdc25A, and COX-2). In reciprocal immunoprecipitation/blotting experiments, phosphorylated Stat3 coimmunoprecipitated with PKCε. As observed in vivo using PKCε knockout mice and in vitro in an immunocomplex kinase assay, PKCε phosphorylated Stat3 at Ser727 residue. These results indicate for the first time that (a) PKCε is a Stat3Ser727 kinase; (b) PKCε-mediated phosphorylation of StatSer727 may be essential for transcriptional activity of Stat3; and (c) UVR-induced phosphorylation of Ser727 may be a key component of the mechanism by which PKCε imparts sensitivity to UVR-induced development of SCC. [Cancer Res 2007;67(3):1385–94] |
Author | AZIZ, Moammir H VERMA, Ajit K MANOHARAN, Herbert T |
Author_xml | – sequence: 1 givenname: Moammir H surname: AZIZ fullname: AZIZ, Moammir H organization: Department of Human Oncology, School of Medicine and Public Health, University of Wisconsin, Madison, Wisconsin, United States – sequence: 2 givenname: Herbert T surname: MANOHARAN fullname: MANOHARAN, Herbert T organization: Department of Human Oncology, School of Medicine and Public Health, University of Wisconsin, Madison, Wisconsin, United States – sequence: 3 givenname: Ajit K surname: VERMA fullname: VERMA, Ajit K organization: Department of Human Oncology, School of Medicine and Public Health, University of Wisconsin, Madison, Wisconsin, United States |
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Keywords | Squamous cell carcinoma Enzyme Protein kinase Toxicity Transferases Transcription factor STAT3 Skin Malignant tumor Sun Radiation damage |
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Snippet | Chronic exposure to UV radiation (UVR) is the major etiologic factor in the development of human skin cancers including squamous cell carcinoma (SCC). We have... Abstract Chronic exposure to UV radiation (UVR) is the major etiologic factor in the development of human skin cancers including squamous cell carcinoma (SCC).... |
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SubjectTerms | Animals Antineoplastic agents Biological and medical sciences Carcinoma, Squamous Cell - enzymology Carcinoma, Squamous Cell - etiology Carcinoma, Squamous Cell - genetics Carcinoma, Squamous Cell - metabolism Enzyme Activation Female Gene Expression Regulation, Neoplastic Male Medical sciences Mice Mice, Inbred C57BL Mice, Knockout Mice, Transgenic Pharmacology. Drug treatments Phosphorylation Protein Kinase C-epsilon - biosynthesis Protein Kinase C-epsilon - genetics Protein Kinase C-epsilon - metabolism Skin - enzymology Skin - radiation effects Skin Neoplasms - enzymology Skin Neoplasms - etiology Skin Neoplasms - genetics Skin Neoplasms - metabolism STAT3 Transcription Factor - genetics STAT3 Transcription Factor - metabolism Tumors Ultraviolet Rays |
Title | Protein kinase Cε, which sensitizes skin to sun's UV radiation-induced cutaneous damage and development of squamous cell carcinomas, associates with stat3 |
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