Altered levels of endogenous retrovirus-like sequence (VL30) RNA during mouse epidermal cell carcinogenesis

K. A. Han, P. Rothberg, Molly Kulesz-Martin

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Gene expression during mouse keratinocyte carcinogenesis was examined in a clonal cell model. Tumor cells from three separate initiated cell lineages were compared with their nontumorigenic precursors and with the progenitor cell strain prior to treatment with 7,12-dimethylbenz[a]anthracene (DMBA). The steady-state levels of VL30 RNA in normal and papilloma cells were regulated by extracellular CA2+ (which controls proliferation and differentiation in normal epidermal keratinocytes) and culture density. In contrast, steady-state levels of VL30 RNA were not regulated by these factors in the squamous cell carcinoma or the anaplastic carcinoma cells. VL30 expression was Ca2+ dependent in the initiated cell precursors within each tumor cell lineage, suggesting that the loss of response to extracellular Ca2+ was associated with the malignant conversion stage of carcinogenesis. No differences between normal and tumor cells were found in the cellular RNA levels of five additional proto-oncogenes. The mouse epidermal cell model should provide a means for direct assessment of a potential functional role of VL30 sequences in cancer development.

Original languageEnglish (US)
Pages (from-to)75-82
Number of pages8
JournalMolecular Carcinogenesis
Volume3
Issue number2
DOIs
StatePublished - 1990
Externally publishedYes

Fingerprint

Endogenous Retroviruses
Carcinogenesis
Cell Lineage
RNA
Keratinocytes
Neoplasms
9,10-Dimethyl-1,2-benzanthracene
Proto-Oncogenes
Papilloma
Squamous Cell Carcinoma
Stem Cells
Carcinoma
Gene Expression

Keywords

  • cell differentiation
  • epithelial carcinogenesis
  • Gene expression

ASJC Scopus subject areas

  • Cancer Research
  • Molecular Biology

Cite this

Altered levels of endogenous retrovirus-like sequence (VL30) RNA during mouse epidermal cell carcinogenesis. / Han, K. A.; Rothberg, P.; Kulesz-Martin, Molly.

In: Molecular Carcinogenesis, Vol. 3, No. 2, 1990, p. 75-82.

Research output: Contribution to journalArticle

@article{f14507c6da674ed482e6f756d149a22f,
title = "Altered levels of endogenous retrovirus-like sequence (VL30) RNA during mouse epidermal cell carcinogenesis",
abstract = "Gene expression during mouse keratinocyte carcinogenesis was examined in a clonal cell model. Tumor cells from three separate initiated cell lineages were compared with their nontumorigenic precursors and with the progenitor cell strain prior to treatment with 7,12-dimethylbenz[a]anthracene (DMBA). The steady-state levels of VL30 RNA in normal and papilloma cells were regulated by extracellular CA2+ (which controls proliferation and differentiation in normal epidermal keratinocytes) and culture density. In contrast, steady-state levels of VL30 RNA were not regulated by these factors in the squamous cell carcinoma or the anaplastic carcinoma cells. VL30 expression was Ca2+ dependent in the initiated cell precursors within each tumor cell lineage, suggesting that the loss of response to extracellular Ca2+ was associated with the malignant conversion stage of carcinogenesis. No differences between normal and tumor cells were found in the cellular RNA levels of five additional proto-oncogenes. The mouse epidermal cell model should provide a means for direct assessment of a potential functional role of VL30 sequences in cancer development.",
keywords = "cell differentiation, epithelial carcinogenesis, Gene expression",
author = "Han, {K. A.} and P. Rothberg and Molly Kulesz-Martin",
year = "1990",
doi = "10.1002/mc.2940030205",
language = "English (US)",
volume = "3",
pages = "75--82",
journal = "Molecular Carcinogenesis",
issn = "0899-1987",
publisher = "Wiley-Liss Inc.",
number = "2",

}

TY - JOUR

T1 - Altered levels of endogenous retrovirus-like sequence (VL30) RNA during mouse epidermal cell carcinogenesis

AU - Han, K. A.

AU - Rothberg, P.

AU - Kulesz-Martin, Molly

PY - 1990

Y1 - 1990

N2 - Gene expression during mouse keratinocyte carcinogenesis was examined in a clonal cell model. Tumor cells from three separate initiated cell lineages were compared with their nontumorigenic precursors and with the progenitor cell strain prior to treatment with 7,12-dimethylbenz[a]anthracene (DMBA). The steady-state levels of VL30 RNA in normal and papilloma cells were regulated by extracellular CA2+ (which controls proliferation and differentiation in normal epidermal keratinocytes) and culture density. In contrast, steady-state levels of VL30 RNA were not regulated by these factors in the squamous cell carcinoma or the anaplastic carcinoma cells. VL30 expression was Ca2+ dependent in the initiated cell precursors within each tumor cell lineage, suggesting that the loss of response to extracellular Ca2+ was associated with the malignant conversion stage of carcinogenesis. No differences between normal and tumor cells were found in the cellular RNA levels of five additional proto-oncogenes. The mouse epidermal cell model should provide a means for direct assessment of a potential functional role of VL30 sequences in cancer development.

AB - Gene expression during mouse keratinocyte carcinogenesis was examined in a clonal cell model. Tumor cells from three separate initiated cell lineages were compared with their nontumorigenic precursors and with the progenitor cell strain prior to treatment with 7,12-dimethylbenz[a]anthracene (DMBA). The steady-state levels of VL30 RNA in normal and papilloma cells were regulated by extracellular CA2+ (which controls proliferation and differentiation in normal epidermal keratinocytes) and culture density. In contrast, steady-state levels of VL30 RNA were not regulated by these factors in the squamous cell carcinoma or the anaplastic carcinoma cells. VL30 expression was Ca2+ dependent in the initiated cell precursors within each tumor cell lineage, suggesting that the loss of response to extracellular Ca2+ was associated with the malignant conversion stage of carcinogenesis. No differences between normal and tumor cells were found in the cellular RNA levels of five additional proto-oncogenes. The mouse epidermal cell model should provide a means for direct assessment of a potential functional role of VL30 sequences in cancer development.

KW - cell differentiation

KW - epithelial carcinogenesis

KW - Gene expression

UR - http://www.scopus.com/inward/record.url?scp=0025374313&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025374313&partnerID=8YFLogxK

U2 - 10.1002/mc.2940030205

DO - 10.1002/mc.2940030205

M3 - Article

VL - 3

SP - 75

EP - 82

JO - Molecular Carcinogenesis

JF - Molecular Carcinogenesis

SN - 0899-1987

IS - 2

ER -