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PMID: 2157183 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Adenovirus E1A represses protease gene expression and inhibits metastasis of human tumor cells.

Oncogene ·Vol. 5 ·No. 1 ·1990-01-00 ·Pages 75-83

Frisch SM, Reich R, Collier IE, Genrich LT, Martin G, Goldberg GI

Abstract

Stable transfection of human tumor cell lines with the adenovirus-5 E1A gene repressed the expression of the secreted proteases, type IV collagenase, interstitial collagenase and urokinase. In addition, E1A blocked the 12-O-tetradecanoyl phorbol acetate (TPA) induction of interstitial collagenase transcription in HT1080 fibrosarcoma cells. Plasmids bearing the interstitial collagenase or type IV collagenase 5' flanking regions linked to a chloramphenicol acetyl transferase coding sequence were constructed and analysed for expression by transient cotransfections into HT1080 cells. Cotransfection with a plasmid bearing a functional E1A gene repressed transcription of the type IV collagenase promoter and blocked the TPA induction of the interstitial collagenase promoter. Furthermore, E1A repressed transcription from a TK promoter driven by AP-1 complex binding sites (TRE), suggesting that E1A interferes with the AP-1 trans-activation pathway. This effect was not, however, due to the repression of c-jun gene transcription by E1A. In fact, the expression of E1A rendered the c-jun gene hypersensitive to TPA induction. Concomitant with reduction in expression levels of secreted proteases, stable E1A transfectants showed reduced metastatic activity in vivo and reduced ability to traverse a reconstituted basement membrane in vitro. Monospecific anti-type IV collagenase antibodies inhibited invasive activity of parental tumor cell lines in the in vitro assay, suggesting a possible causal relationship between the repression of secreted proteases and loss of metastatic properties of the transformants.

MeSH Terms
Adenovirus Early Proteins Base Sequence Cell Transformation, Neoplastic Chloramphenicol O-Acetyltransferase/analysis,genetics DNA-Binding Proteins/genetics Gene Expression Humans Metalloendopeptidases/genetics Microbial Collagenase/genetics Molecular Sequence Data Neoplasm Invasiveness Neoplasm Metastasis Oncogene Proteins, Viral/physiology Peptide Hydrolases/genetics,physiology Proto-Oncogene Proteins c-jun Proto-Oncogenes Tetradecanoylphorbol Acetate/pharmacology Transcription Factors/genetics Transcription, Genetic Transfection
Chemicals
Adenovirus Early Proteins DNA-Binding Proteins Oncogene Proteins, Viral Proto-Oncogene Proteins c-jun Transcription Factors Chloramphenicol O-Acetyltransferase Peptide Hydrolases Metalloendopeptidases Microbial Collagenase Tetradecanoylphorbol Acetate
Authors & Affiliations
6 authors, click to expand affiliations / ORCID
Frisch S M
Division of Dermatology, Washington University School of Medicine, St. Louis, Missouri 63110.
Reich R
Collier I E
Genrich L T
Martin G
Goldberg G I
Article Info
Journal
Oncogene
Abbr.
Oncogene
ISSN
0950-9232
Published
1990-01-00
Pages
75-83
Language
English
Region
England
NLM ID
8711562
Subset
IM
Grants
NIAMS NIH HHS · AR 12129 · United States
NIAMS NIH HHS · AR 39472 · United States
NIADDK NIH HHS · TO-AM07284 · United States
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