Identification of differentially expressed genes in chemically induced skin tumors

Susan E. Rutberg, Edwin J. Lee, Laura A. Hansen, Adam B. Glick, Stuart H. Yuspa

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Previous studies have demonstrated a role for the fos gene in promoting malignant conversion of mouse skin tumors. In the study reported here, differential display was performed to identify fos- and jun-regulated genes that are differentially expressed during premalignant progression. Total RNA isolated from variants of the papilloma cell line SP-1 transduced with retroviral vectors expressing v-jun and v-fos alone or in tandem was analyzed for the presence of differentially expressed transcripts by using 35 different primer combinations. Differentially expressed clones were rescreened by dot-blot analysis by using cDNA from chemically induced tumors with a high or low risk of malignant conversion. Three differentially displayed fragments were isolated in this analysis. Homology searches indicated that these fragments shared significant homology with the apoptosis inhibitor bcl-2, human alternative splicing factor/splicing factor 2 (ASF/SF2), and a novel gene not present in the GenBank or EMBL databases. In situ hybridization indicated that the expression levels of the bcl-2 homolog increased with malignant potential in chemically derived mouse skin tumors. A similar analysis indicated that expression of the ASF/SF2 homolog was greater in papillomas than in normal skin or in squamous cell carcinomas. Transcripts for this gene were most abundant in the granular layer. The expression pattern of the third differential display fragment was consistent with that of a tumor suppressor gene. This gene was expressed at very high levels in normal skin and benign papillomas but was essentially undetectable in squamous cell carcinomas. Through this approach, we identified known and novel genes that may contribute to malignant progression in epidermal tumors.

Original languageEnglish
Pages (from-to)88-98
Number of pages11
JournalMolecular Carcinogenesis
Volume20
Issue number1
DOIs
StatePublished - Sep 1997
Externally publishedYes

Fingerprint

Papilloma
Skin
Alternative Splicing
Genes
Squamous Cell Carcinoma
Neoplasms
jun Genes
fos Genes
Nucleic Acid Databases
Tumor Suppressor Genes
In Situ Hybridization
Complementary DNA
Clone Cells
Databases
RNA
Apoptosis
Cell Line
RNA Splicing Factors

All Science Journal Classification (ASJC) codes

  • Cancer Research
  • Molecular Biology

Cite this

Identification of differentially expressed genes in chemically induced skin tumors. / Rutberg, Susan E.; Lee, Edwin J.; Hansen, Laura A.; Glick, Adam B.; Yuspa, Stuart H.

In: Molecular Carcinogenesis, Vol. 20, No. 1, 09.1997, p. 88-98.

Research output: Contribution to journalArticle

Rutberg, Susan E. ; Lee, Edwin J. ; Hansen, Laura A. ; Glick, Adam B. ; Yuspa, Stuart H. / Identification of differentially expressed genes in chemically induced skin tumors. In: Molecular Carcinogenesis. 1997 ; Vol. 20, No. 1. pp. 88-98.
@article{7b4e62353c224aaf90aaac0e03457701,
title = "Identification of differentially expressed genes in chemically induced skin tumors",
abstract = "Previous studies have demonstrated a role for the fos gene in promoting malignant conversion of mouse skin tumors. In the study reported here, differential display was performed to identify fos- and jun-regulated genes that are differentially expressed during premalignant progression. Total RNA isolated from variants of the papilloma cell line SP-1 transduced with retroviral vectors expressing v-jun and v-fos alone or in tandem was analyzed for the presence of differentially expressed transcripts by using 35 different primer combinations. Differentially expressed clones were rescreened by dot-blot analysis by using cDNA from chemically induced tumors with a high or low risk of malignant conversion. Three differentially displayed fragments were isolated in this analysis. Homology searches indicated that these fragments shared significant homology with the apoptosis inhibitor bcl-2, human alternative splicing factor/splicing factor 2 (ASF/SF2), and a novel gene not present in the GenBank or EMBL databases. In situ hybridization indicated that the expression levels of the bcl-2 homolog increased with malignant potential in chemically derived mouse skin tumors. A similar analysis indicated that expression of the ASF/SF2 homolog was greater in papillomas than in normal skin or in squamous cell carcinomas. Transcripts for this gene were most abundant in the granular layer. The expression pattern of the third differential display fragment was consistent with that of a tumor suppressor gene. This gene was expressed at very high levels in normal skin and benign papillomas but was essentially undetectable in squamous cell carcinomas. Through this approach, we identified known and novel genes that may contribute to malignant progression in epidermal tumors.",
author = "Rutberg, {Susan E.} and Lee, {Edwin J.} and Hansen, {Laura A.} and Glick, {Adam B.} and Yuspa, {Stuart H.}",
year = "1997",
month = "9",
doi = "10.1002/(SICI)1098-2744(199709)20:1<88::AID-MC10>3.0.CO;2-5",
language = "English",
volume = "20",
pages = "88--98",
journal = "Molecular Carcinogenesis",
issn = "0899-1987",
publisher = "Wiley-Liss Inc.",
number = "1",

}

TY - JOUR

T1 - Identification of differentially expressed genes in chemically induced skin tumors

AU - Rutberg, Susan E.

AU - Lee, Edwin J.

AU - Hansen, Laura A.

AU - Glick, Adam B.

AU - Yuspa, Stuart H.

PY - 1997/9

Y1 - 1997/9

N2 - Previous studies have demonstrated a role for the fos gene in promoting malignant conversion of mouse skin tumors. In the study reported here, differential display was performed to identify fos- and jun-regulated genes that are differentially expressed during premalignant progression. Total RNA isolated from variants of the papilloma cell line SP-1 transduced with retroviral vectors expressing v-jun and v-fos alone or in tandem was analyzed for the presence of differentially expressed transcripts by using 35 different primer combinations. Differentially expressed clones were rescreened by dot-blot analysis by using cDNA from chemically induced tumors with a high or low risk of malignant conversion. Three differentially displayed fragments were isolated in this analysis. Homology searches indicated that these fragments shared significant homology with the apoptosis inhibitor bcl-2, human alternative splicing factor/splicing factor 2 (ASF/SF2), and a novel gene not present in the GenBank or EMBL databases. In situ hybridization indicated that the expression levels of the bcl-2 homolog increased with malignant potential in chemically derived mouse skin tumors. A similar analysis indicated that expression of the ASF/SF2 homolog was greater in papillomas than in normal skin or in squamous cell carcinomas. Transcripts for this gene were most abundant in the granular layer. The expression pattern of the third differential display fragment was consistent with that of a tumor suppressor gene. This gene was expressed at very high levels in normal skin and benign papillomas but was essentially undetectable in squamous cell carcinomas. Through this approach, we identified known and novel genes that may contribute to malignant progression in epidermal tumors.

AB - Previous studies have demonstrated a role for the fos gene in promoting malignant conversion of mouse skin tumors. In the study reported here, differential display was performed to identify fos- and jun-regulated genes that are differentially expressed during premalignant progression. Total RNA isolated from variants of the papilloma cell line SP-1 transduced with retroviral vectors expressing v-jun and v-fos alone or in tandem was analyzed for the presence of differentially expressed transcripts by using 35 different primer combinations. Differentially expressed clones were rescreened by dot-blot analysis by using cDNA from chemically induced tumors with a high or low risk of malignant conversion. Three differentially displayed fragments were isolated in this analysis. Homology searches indicated that these fragments shared significant homology with the apoptosis inhibitor bcl-2, human alternative splicing factor/splicing factor 2 (ASF/SF2), and a novel gene not present in the GenBank or EMBL databases. In situ hybridization indicated that the expression levels of the bcl-2 homolog increased with malignant potential in chemically derived mouse skin tumors. A similar analysis indicated that expression of the ASF/SF2 homolog was greater in papillomas than in normal skin or in squamous cell carcinomas. Transcripts for this gene were most abundant in the granular layer. The expression pattern of the third differential display fragment was consistent with that of a tumor suppressor gene. This gene was expressed at very high levels in normal skin and benign papillomas but was essentially undetectable in squamous cell carcinomas. Through this approach, we identified known and novel genes that may contribute to malignant progression in epidermal tumors.

UR - http://www.scopus.com/inward/record.url?scp=0030783657&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030783657&partnerID=8YFLogxK

U2 - 10.1002/(SICI)1098-2744(199709)20:1<88::AID-MC10>3.0.CO;2-5

DO - 10.1002/(SICI)1098-2744(199709)20:1<88::AID-MC10>3.0.CO;2-5

M3 - Article

VL - 20

SP - 88

EP - 98

JO - Molecular Carcinogenesis

JF - Molecular Carcinogenesis

SN - 0899-1987

IS - 1

ER -