VILIP-1 expression in vivo results in decreased mouse skin keratinocyte proliferation and tumor development

VILIP-1, a member of the neuronal Ca(2+) sensor protein family, is able to act as a tumor suppressor in carcinoma cells by inhibiting cell proliferation and migration. In order to study the role of VILIP-1 in skin carcinogenesis we generated transgenic mice overexpressing VILIP-1 in epidermis under...

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Published in:PloS one 2010-04, Vol.5 (4), p.e10196
Main Authors: Fu, Jian, Jin, Fang, Zhang, Jirong, Fong, Kathryn, Bassi, Daniel E, Lopez De Cicco, Ricardo, Ramaraju, Divya, Braunewell, Karl-Heinz, Conti, Claudio, Benavides, Fernando, Klein-Szanto, Andres J P
Format: Article
Language:English
Subjects:
Adenosine triphosphatase
Animal models
Animals
Apoptosis
Benzo(a)pyrene
Biochemistry/Chemical Biology of the Cell
Biology
Calcium
Cancer
Carcinogenesis
Carcinogens
Carcinoma, Squamous Cell - etiology
Carcinoma, Squamous Cell - pathology
Cell Biology/Chemical Biology of the Cell
Cell Proliferation
Deoxyribonucleic acid
Disease Susceptibility
DNA
Epidermis
Gelatinase B
Genes, Tumor Suppressor
Genetic engineering
Keratin
Keratinocytes
Keratinocytes - cytology
Matrix metalloproteinase
Matrix Metalloproteinase 9
Metalloproteinase
Metastasis
Mice
Mice, Transgenic
Molecular weight
Neurocalcin
Neurocalcin - genetics
Neurocalcin - physiology
Neurons
Oncology/Skin Cancers
Pathology
Pathology/Cellular Pathology
Proteins
Pyrene
Rodents
Skin
Skin cancer
Skin Neoplasms - etiology
Skin Neoplasms - pathology
Squamous cell carcinoma
Tissue Inhibitor of Metalloproteinase-1
Transgenic animals
Transgenic mice
Tumor suppressor genes
Tumor Suppressor Proteins - genetics
Tumors
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container_issue 4
container_start_page e10196
container_title PloS one
container_volume 5
creator Fu, Jian
Jin, Fang
Zhang, Jirong
Fong, Kathryn
Bassi, Daniel E
Lopez De Cicco, Ricardo
Ramaraju, Divya
Braunewell, Karl-Heinz
Conti, Claudio
Benavides, Fernando
Klein-Szanto, Andres J P
description VILIP-1, a member of the neuronal Ca(2+) sensor protein family, is able to act as a tumor suppressor in carcinoma cells by inhibiting cell proliferation and migration. In order to study the role of VILIP-1 in skin carcinogenesis we generated transgenic mice overexpressing VILIP-1 in epidermis under the control of the bovine keratin K5 promoter (K5-VILIP-1). We studied the susceptibility of FVB wild type and VILIP-1 transgenic mice to chemically mediated carcinogenesis. After 30 weeks of treatment with a two-stage carcinogenesis protocol, all animals showed numerous skin tumors. Nevertheless, K5-VILIP-1 mice showed decreased squamous cell carcinoma (SCC) multiplicity of approximately 49% (p
doi_str_mv 10.1371/journal.pone.0010196
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In order to study the role of VILIP-1 in skin carcinogenesis we generated transgenic mice overexpressing VILIP-1 in epidermis under the control of the bovine keratin K5 promoter (K5-VILIP-1). We studied the susceptibility of FVB wild type and VILIP-1 transgenic mice to chemically mediated carcinogenesis. After 30 weeks of treatment with a two-stage carcinogenesis protocol, all animals showed numerous skin tumors. Nevertheless, K5-VILIP-1 mice showed decreased squamous cell carcinoma (SCC) multiplicity of approximately 49% (p&lt;0.02) with respect to the corresponding SCC multiplicity observed in wild type (WT) mice. In addition, the relative percentage of low-grade cutaneous SCCs grade I (defined by the differentiation pattern according to the Broders grading scale) increased approximately 50% in the K5-VILIP1 mice when compared with SCCs in WT mice. Similar tendency was observed using a complete carcinogenesis protocol for skin carcinogenesis using benzo(a)pyrene (B(a)P). Further studies of tumors and primary epidermal keratinocyte cultures showed that matrix metalloproteinase 9 (MMP-9) levels and cell proliferation decreased in K5-VILIP-1 mice when compared with their wild counterparts. In addition tissue inhibitor of metalloproteinase 1 (TIMP-1) expression was higher in K5-VILIP-1 keratinocytes. These results show that VILIP-1 overexpression decreases the susceptibility to skin carcinogenesis in experimental mouse cancer models, thus supporting its role as a tumor suppressor gene.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0010196</identifier><identifier>PMID: 20419170</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adenosine triphosphatase ; Animal models ; Animals ; Apoptosis ; Benzo(a)pyrene ; Biochemistry/Chemical Biology of the Cell ; Biology ; Calcium ; Cancer ; Carcinogenesis ; Carcinogens ; Carcinoma, Squamous Cell - etiology ; Carcinoma, Squamous Cell - pathology ; Cell Biology/Chemical Biology of the Cell ; Cell Proliferation ; Deoxyribonucleic acid ; Disease Susceptibility ; DNA ; Epidermis ; Gelatinase B ; Genes, Tumor Suppressor ; Genetic engineering ; Keratin ; Keratinocytes ; Keratinocytes - cytology ; Matrix metalloproteinase ; Matrix Metalloproteinase 9 ; Metalloproteinase ; Metastasis ; Mice ; Mice, Transgenic ; Molecular weight ; Neurocalcin ; Neurocalcin - genetics ; Neurocalcin - physiology ; Neurons ; Oncology/Skin Cancers ; Pathology ; Pathology/Cellular Pathology ; Proteins ; Pyrene ; Rodents ; Skin ; Skin cancer ; Skin Neoplasms - etiology ; Skin Neoplasms - pathology ; Squamous cell carcinoma ; Tissue Inhibitor of Metalloproteinase-1 ; Transgenic animals ; Transgenic mice ; Tumor suppressor genes ; Tumor Suppressor Proteins - genetics ; Tumors</subject><ispartof>PloS one, 2010-04, Vol.5 (4), p.e10196</ispartof><rights>COPYRIGHT 2010 Public Library of Science</rights><rights>2010 Fu et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. 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In order to study the role of VILIP-1 in skin carcinogenesis we generated transgenic mice overexpressing VILIP-1 in epidermis under the control of the bovine keratin K5 promoter (K5-VILIP-1). We studied the susceptibility of FVB wild type and VILIP-1 transgenic mice to chemically mediated carcinogenesis. After 30 weeks of treatment with a two-stage carcinogenesis protocol, all animals showed numerous skin tumors. Nevertheless, K5-VILIP-1 mice showed decreased squamous cell carcinoma (SCC) multiplicity of approximately 49% (p&lt;0.02) with respect to the corresponding SCC multiplicity observed in wild type (WT) mice. In addition, the relative percentage of low-grade cutaneous SCCs grade I (defined by the differentiation pattern according to the Broders grading scale) increased approximately 50% in the K5-VILIP1 mice when compared with SCCs in WT mice. Similar tendency was observed using a complete carcinogenesis protocol for skin carcinogenesis using benzo(a)pyrene (B(a)P). Further studies of tumors and primary epidermal keratinocyte cultures showed that matrix metalloproteinase 9 (MMP-9) levels and cell proliferation decreased in K5-VILIP-1 mice when compared with their wild counterparts. In addition tissue inhibitor of metalloproteinase 1 (TIMP-1) expression was higher in K5-VILIP-1 keratinocytes. These results show that VILIP-1 overexpression decreases the susceptibility to skin carcinogenesis in experimental mouse cancer models, thus supporting its role as a tumor suppressor gene.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>20419170</pmid><doi>10.1371/journal.pone.0010196</doi><tpages>e10196</tpages><oa>free_for_read</oa></addata></record>
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identifier ISSN: 1932-6203
ispartof PloS one, 2010-04, Vol.5 (4), p.e10196
issn 1932-6203
1932-6203
language eng
recordid cdi_plos_journals_1289453513
source NCBI_PubMed Central（免费）; Publicly Available Content (ProQuest)
subjects Adenosine triphosphatase
Animal models
Animals
Apoptosis
Benzo(a)pyrene
Biochemistry/Chemical Biology of the Cell
Biology
Calcium
Cancer
Carcinogenesis
Carcinogens
Carcinoma, Squamous Cell - etiology
Carcinoma, Squamous Cell - pathology
Cell Biology/Chemical Biology of the Cell
Cell Proliferation
Deoxyribonucleic acid
Disease Susceptibility
DNA
Epidermis
Gelatinase B
Genes, Tumor Suppressor
Genetic engineering
Keratin
Keratinocytes
Keratinocytes - cytology
Matrix metalloproteinase
Matrix Metalloproteinase 9
Metalloproteinase
Metastasis
Mice
Mice, Transgenic
Molecular weight
Neurocalcin
Neurocalcin - genetics
Neurocalcin - physiology
Neurons
Oncology/Skin Cancers
Pathology
Pathology/Cellular Pathology
Proteins
Pyrene
Rodents
Skin
Skin cancer
Skin Neoplasms - etiology
Skin Neoplasms - pathology
Squamous cell carcinoma
Tissue Inhibitor of Metalloproteinase-1
Transgenic animals
Transgenic mice
Tumor suppressor genes
Tumor Suppressor Proteins - genetics
Tumors
title VILIP-1 expression in vivo results in decreased mouse skin keratinocyte proliferation and tumor development
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