Genetic deletion of TNFα inhibits ultraviolet radiation-induced development of cutaneous squamous cell carcinomas in PKCε transgenic mice via inhibition of cell survival signals
Protein kinase C epsilon (PKCε), a Ca(2+)-independent phospholipid-dependent serine/threonine kinase, is among the six PKC isoforms (α, δ, ε, η, μ, ζ) expressed in both mouse and human skin. Epidermal PKCε level dictates the susceptibility of PKCε transgenic (TG) mice to the development of cutaneous...
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Published in | Carcinogenesis (New York) Vol. 37; no. 1; pp. 72 - 80 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
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Oxford University Press
01.01.2016
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Abstract | Protein kinase C epsilon (PKCε), a Ca(2+)-independent phospholipid-dependent serine/threonine kinase, is among the six PKC isoforms (α, δ, ε, η, μ, ζ) expressed in both mouse and human skin. Epidermal PKCε level dictates the susceptibility of PKCε transgenic (TG) mice to the development of cutaneous squamous cell carcinomas (SCC) elicited either by repeated exposure to ultraviolet radiation (UVR) or by using the DMBA initiation-TPA (12-O-tetradecanoylphorbol-13-acetate) tumor promotion protocol (Wheeler,D.L. et al. (2004) Protein kinase C epsilon is an endogenous photosensitizer that enhances ultraviolet radiation-induced cutaneous damage and development of squamous cell carcinomas. Cancer Res., 64, 7756-7765). Histologically, SCC in TG mice, like human SCC, is poorly differentiated and metastatic. Our earlier studies to elucidate mechanisms of PKCε-mediated development of SCC, using either DMBA-TPA or UVR, indicated elevated release of cytokine TNFα. To determine whether TNFα is essential for the development of SCC in TG mice, we generated PKCε transgenic mice/TNFα-knockout (TG/TNFαKO) by crossbreeding TNFαKO with TG mice. We now present that deletion of TNFα in TG mice inhibited the development of SCC either by repeated UVR exposures or by the DMBA-TPA protocol. TG mice deficient in TNFα elicited both increase in SCC latency and decrease in SCC incidence. Inhibition of UVR-induced SCC development in TG/TNFαKO was accompanied by inhibition of (i) the expression levels of TNFα receptors TNFRI and TNFRII and cell proliferation marker ornithine decarboxylase and metastatic markers MMP7 and MMP9, (ii) the activation of transcription factors Stat3 and NF-kB and (iii) proliferation of hair follicle stem cells and epidermal hyperplasia. The results presented here provide the first genetic evidence that TNFα is linked to PKCε-mediated sensitivity to DMBA-TPA or UVR-induced development of cutaneous SCC. |
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AbstractList | This study presents that deletion of TNF-α in PKC epsilon transgenic mice inhibits the development of cutaneous SCCs elicited either by repeated ultraviolet radiation exposures or by the DMBA initiation-TPA promotion protocol via inhibition of survival signals to epidermal cell proliferation including HSCs.
Protein kinase C epsilon (PKCε), a Ca
2+
-independent phospholipid-dependent serine/threonine kinase, is among the six PKC isoforms (α, δ, ε, η, μ, ζ) expressed in both mouse and human skin. Epidermal PKCε level dictates the susceptibility of PKCε transgenic (TG) mice to the development of cutaneous squamous cell carcinomas (SCC) elicited either by repeated exposure to ultraviolet radiation (UVR) or by using the DMBA initiation-TPA (12-O-tetradecanoylphorbol-13-acetate) tumor promotion protocol (Wheeler,D.L.
et al.
(2004) Protein kinase C epsilon is an endogenous photosensitizer that enhances ultraviolet radiation-induced cutaneous damage and development of squamous cell carcinomas. Cancer Res., 64, 7756–7765). Histologically, SCC in TG mice, like human SCC, is poorly differentiated and metastatic. Our earlier studies to elucidate mechanisms of PKCε-mediated development of SCC, using either DMBA-TPA or UVR, indicated elevated release of cytokine TNFα. To determine whether TNFα is essential for the development of SCC in TG mice, we generated PKCε transgenic mice/TNFα-knockout (TG/TNFαKO) by crossbreeding TNFαKO with TG mice. We now present that deletion of TNFα in TG mice inhibited the development of SCC either by repeated UVR exposures or by the DMBA-TPA protocol. TG mice deficient in TNFα elicited both increase in SCC latency and decrease in SCC incidence. Inhibition of UVR-induced SCC development in TG/TNFαKO was accompanied by inhibition of (i) the expression levels of TNFα receptors TNFRI and TNFRII and cell proliferation marker ornithine decarboxylase and metastatic markers MMP7 and MMP9, (ii) the activation of transcription factors Stat3 and NF-kB and (iii) proliferation of hair follicle stem cells and epidermal hyperplasia. The results presented here provide the first genetic evidence that TNFα is linked to PKCε-mediated sensitivity to DMBA-TPA or UVR-induced development of cutaneous SCC. Protein kinase C epsilon (PKCε), a Ca(2+)-independent phospholipid-dependent serine/threonine kinase, is among the six PKC isoforms (α, δ, ε, η, μ, ζ) expressed in both mouse and human skin. Epidermal PKCε level dictates the susceptibility of PKCε transgenic (TG) mice to the development of cutaneous squamous cell carcinomas (SCC) elicited either by repeated exposure to ultraviolet radiation (UVR) or by using the DMBA initiation-TPA (12-O-tetradecanoylphorbol-13-acetate) tumor promotion protocol (Wheeler,D.L. et al. (2004) Protein kinase C epsilon is an endogenous photosensitizer that enhances ultraviolet radiation-induced cutaneous damage and development of squamous cell carcinomas. Cancer Res., 64, 7756-7765). Histologically, SCC in TG mice, like human SCC, is poorly differentiated and metastatic. Our earlier studies to elucidate mechanisms of PKCε-mediated development of SCC, using either DMBA-TPA or UVR, indicated elevated release of cytokine TNFα. To determine whether TNFα is essential for the development of SCC in TG mice, we generated PKCε transgenic mice/TNFα-knockout (TG/TNFαKO) by crossbreeding TNFαKO with TG mice. We now present that deletion of TNFα in TG mice inhibited the development of SCC either by repeated UVR exposures or by the DMBA-TPA protocol. TG mice deficient in TNFα elicited both increase in SCC latency and decrease in SCC incidence. Inhibition of UVR-induced SCC development in TG/TNFαKO was accompanied by inhibition of (i) the expression levels of TNFα receptors TNFRI and TNFRII and cell proliferation marker ornithine decarboxylase and metastatic markers MMP7 and MMP9, (ii) the activation of transcription factors Stat3 and NF-kB and (iii) proliferation of hair follicle stem cells and epidermal hyperplasia. The results presented here provide the first genetic evidence that TNFα is linked to PKCε-mediated sensitivity to DMBA-TPA or UVR-induced development of cutaneous SCC. |
Author | Kim, KyungMann Wheeler, Deric L Havighurst, Thomas C Bauer, Samuel J Verma, Ajit K Singh, Ashok Singh, Anupama |
Author_xml | – sequence: 1 givenname: Ashok surname: Singh fullname: Singh, Ashok – sequence: 2 givenname: Anupama surname: Singh fullname: Singh, Anupama – sequence: 3 givenname: Samuel J surname: Bauer fullname: Bauer, Samuel J – sequence: 4 givenname: Deric L surname: Wheeler fullname: Wheeler, Deric L – sequence: 5 givenname: Thomas C surname: Havighurst fullname: Havighurst, Thomas C organization: Department of Biostatistics and Medical Informatics, Paul P. Carbone Comprehensive Cancer Center, School of Medicine and Public Health, University of Wisconsin, Madison, WI 53792, USA – sequence: 6 givenname: KyungMann surname: Kim fullname: Kim, KyungMann organization: Department of Biostatistics and Medical Informatics, Paul P. Carbone Comprehensive Cancer Center, School of Medicine and Public Health, University of Wisconsin, Madison, WI 53792, USA – sequence: 7 givenname: Ajit K surname: Verma fullname: Verma, Ajit K |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26586792$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_1038_s41388_020_1323_3 crossref_primary_10_18632_oncotarget_25768 crossref_primary_10_1038_s41418_023_01153_w crossref_primary_10_1007_s00403_020_02102_0 crossref_primary_10_1007_s11756_022_01018_6 crossref_primary_10_1007_s00403_019_01939_4 crossref_primary_10_1080_08820139_2016_1197242 crossref_primary_10_3390_life11040326 crossref_primary_10_7759_cureus_38596 crossref_primary_10_5334_1750_2187_11_2 |
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Snippet | Protein kinase C epsilon (PKCε), a Ca(2+)-independent phospholipid-dependent serine/threonine kinase, is among the six PKC isoforms (α, δ, ε, η, μ, ζ)... This study presents that deletion of TNF-α in PKC epsilon transgenic mice inhibits the development of cutaneous SCCs elicited either by repeated ultraviolet... |
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SubjectTerms | 9,10-Dimethyl-1,2-benzanthracene Animals Carcinogenesis - chemically induced Carcinogenesis - genetics Carcinogenesis - radiation effects Carcinogens Carcinoma, Squamous Cell - etiology Carcinoma, Squamous Cell - genetics Carcinoma, Squamous Cell - metabolism Carcinoma, Squamous Cell - prevention & control Cell Survival - drug effects Cell Survival - genetics Cell Survival - radiation effects Female Male Mice Mice, Knockout Mice, Transgenic Original Manuscript Protein Kinase C-epsilon - biosynthesis Protein Kinase C-epsilon - genetics Skin Neoplasms - etiology Skin Neoplasms - genetics Skin Neoplasms - metabolism Skin Neoplasms - prevention & control Tetradecanoylphorbol Acetate Tumor Necrosis Factor-alpha - deficiency Tumor Necrosis Factor-alpha - genetics Ultraviolet Rays |
Title | Genetic deletion of TNFα inhibits ultraviolet radiation-induced development of cutaneous squamous cell carcinomas in PKCε transgenic mice via inhibition of cell survival signals |
URI | https://www.ncbi.nlm.nih.gov/pubmed/26586792 https://pubmed.ncbi.nlm.nih.gov/PMC5006113 |
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