DMBA/TPA-induced tumor formation is aggravated in human papillomavirus type 16 E6/E7 transgenic mouse skin

Myoung Ok Kim; Sung Hyun Kim; Mi Jung Shin; Dong Hoon Yu; Bong Soo Kim; Kyu Tae Chang; Sanggyu Lee; Yong Bok Park; Tae Hoon Lee; Zae Young Ryoo

doi:10.3727/000000006783980964

DMBA/TPA-induced tumor formation is aggravated in human papillomavirus type 16 E6/E7 transgenic mouse skin

Myoung Ok Kim, Sung Hyun Kim, Mi Jung Shin, Dong Hoon Yu, Bong Soo Kim, Kyu Tae Chang, Sanggyu Lee, Yong Bok Park, Tae Hoon Lee, Zae Young Ryoo

Research output: Contribution to journal › Article › peer-review

3 Scopus citations

Abstract

Human papillomavirus type 16 (HPV16) is a major causative factor in the development of uterine cervical carcinomas. We investigated the role of E6/E7 in tumor formation. Skin-specific E6/E7 transgenic mice showed approximately twice as many tumors compared with nontransgenic mice in dimethylbenz[a]anthracene (DMBA)-initiated and a 12-O-tetradecanoylphorbol-13-acetate (TPA)-promoted two-stage skin carcinogenesis. This model showed a significant increase of epidermal cell proliferation in the transgenic mice. The 8-hydroxy- 2'deoxyguanosine (8OH-dG) detection assay showed that oxidative DNA damage was significantly higher in the transgenic mice after TPA treatments. The overexpression of E6/E7 in the skin in the DMBA/TPA two-stage-induced carcinogenesis model aggravated the incidence of tumor formation. HPV16 E6/E7 appears to act as an enhancer of carcinogenesis that requires initiation by DMBA and promotion by TPA.

Original language	English
Pages (from-to)	325-332
Number of pages	8
Journal	Oncology Research
Volume	16
Issue number	7
DOIs	https://doi.org/10.3727/000000006783980964
State	Published - 2007

Keywords

DMBA/TPA
HPV16 E6/E7
Keratinocytes
Skin cancer
Transgenic mice
hK14 promoter

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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title = "DMBA/TPA-induced tumor formation is aggravated in human papillomavirus type 16 E6/E7 transgenic mouse skin",

abstract = "Human papillomavirus type 16 (HPV16) is a major causative factor in the development of uterine cervical carcinomas. We investigated the role of E6/E7 in tumor formation. Skin-specific E6/E7 transgenic mice showed approximately twice as many tumors compared with nontransgenic mice in dimethylbenz[a]anthracene (DMBA)-initiated and a 12-O-tetradecanoylphorbol-13-acetate (TPA)-promoted two-stage skin carcinogenesis. This model showed a significant increase of epidermal cell proliferation in the transgenic mice. The 8-hydroxy- 2'deoxyguanosine (8OH-dG) detection assay showed that oxidative DNA damage was significantly higher in the transgenic mice after TPA treatments. The overexpression of E6/E7 in the skin in the DMBA/TPA two-stage-induced carcinogenesis model aggravated the incidence of tumor formation. HPV16 E6/E7 appears to act as an enhancer of carcinogenesis that requires initiation by DMBA and promotion by TPA.",

keywords = "DMBA/TPA, HPV16 E6/E7, Keratinocytes, Skin cancer, Transgenic mice, hK14 promoter",

author = "Kim, {Myoung Ok} and Kim, {Sung Hyun} and Shin, {Mi Jung} and Yu, {Dong Hoon} and Kim, {Bong Soo} and Chang, {Kyu Tae} and Sanggyu Lee and Park, {Yong Bok} and Lee, {Tae Hoon} and Ryoo, {Zae Young}",

year = "2007",

doi = "10.3727/000000006783980964",

language = "English",

volume = "16",

pages = "325--332",

journal = "Oncology Research",

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T1 - DMBA/TPA-induced tumor formation is aggravated in human papillomavirus type 16 E6/E7 transgenic mouse skin

AU - Kim, Myoung Ok

AU - Kim, Sung Hyun

AU - Shin, Mi Jung

AU - Yu, Dong Hoon

AU - Kim, Bong Soo

AU - Chang, Kyu Tae

AU - Lee, Sanggyu

AU - Park, Yong Bok

AU - Lee, Tae Hoon

AU - Ryoo, Zae Young

PY - 2007

Y1 - 2007

N2 - Human papillomavirus type 16 (HPV16) is a major causative factor in the development of uterine cervical carcinomas. We investigated the role of E6/E7 in tumor formation. Skin-specific E6/E7 transgenic mice showed approximately twice as many tumors compared with nontransgenic mice in dimethylbenz[a]anthracene (DMBA)-initiated and a 12-O-tetradecanoylphorbol-13-acetate (TPA)-promoted two-stage skin carcinogenesis. This model showed a significant increase of epidermal cell proliferation in the transgenic mice. The 8-hydroxy- 2'deoxyguanosine (8OH-dG) detection assay showed that oxidative DNA damage was significantly higher in the transgenic mice after TPA treatments. The overexpression of E6/E7 in the skin in the DMBA/TPA two-stage-induced carcinogenesis model aggravated the incidence of tumor formation. HPV16 E6/E7 appears to act as an enhancer of carcinogenesis that requires initiation by DMBA and promotion by TPA.

AB - Human papillomavirus type 16 (HPV16) is a major causative factor in the development of uterine cervical carcinomas. We investigated the role of E6/E7 in tumor formation. Skin-specific E6/E7 transgenic mice showed approximately twice as many tumors compared with nontransgenic mice in dimethylbenz[a]anthracene (DMBA)-initiated and a 12-O-tetradecanoylphorbol-13-acetate (TPA)-promoted two-stage skin carcinogenesis. This model showed a significant increase of epidermal cell proliferation in the transgenic mice. The 8-hydroxy- 2'deoxyguanosine (8OH-dG) detection assay showed that oxidative DNA damage was significantly higher in the transgenic mice after TPA treatments. The overexpression of E6/E7 in the skin in the DMBA/TPA two-stage-induced carcinogenesis model aggravated the incidence of tumor formation. HPV16 E6/E7 appears to act as an enhancer of carcinogenesis that requires initiation by DMBA and promotion by TPA.

KW - DMBA/TPA

KW - HPV16 E6/E7

KW - Keratinocytes

KW - Skin cancer

KW - Transgenic mice

KW - hK14 promoter

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DO - 10.3727/000000006783980964

M3 - Article

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AN - SCOPUS:34250346021

SN - 0965-0407

VL - 16

SP - 325

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JO - Oncology Research

JF - Oncology Research

IS - 7

ER -

DMBA/TPA-induced tumor formation is aggravated in human papillomavirus type 16 E6/E7 transgenic mouse skin

Abstract

Keywords

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