Trapping of genes induced upon growth arrest after treatment with antiestrogen or retinoids using retroviral promoter trap

Soonmyoung Paik, James A. Zwiebel, Marc E Lippman

Research output: Contribution to journalArticle

Abstract

Although chemopreventive anti‐steroids such as the antiestrogens are thought to act through competitive inhibition of agonist binding to estrogen receptors, it has been postulated that the estrogen receptor changes its conformation when bound to a strong antiestrogen such as ICI‐164,384. We hypothesized that such conformationally changed receptors could bind specific recognition sequences in the genome and activate specific genes that might be involved in growth arrest. In order to identify such genes with a functional assay, we used a retroviral gene trap U3lacZ. We have now isolated MCF‐7 breast cancer cell line clones in which the lacZ reporter gene is inserted into the genes activated by either ICI‐164,384 or retinoic acid. One such clone, B4, was further characterized. In B4, lacZ activity is induced by ICI‐164,384 or trans‐retinoic acid, and repressed after treatment with estradiol. Cloning of the 5′‐flanking genomic sequence in this clone will be possible using polymerase chain reaction.

Original languageEnglish (US)
Pages (from-to)254
Number of pages1
JournalJournal of Cellular Biochemistry
Volume53
Issue numberS17G
DOIs
StatePublished - 1993
Externally publishedYes

Fingerprint

Estrogen Receptor Modulators
Retinoids
Genes
Clone Cells
Growth
Estrogen Receptors
Lac Operon
Therapeutics
Tretinoin
Reporter Genes
Organism Cloning
Estradiol
Cloning
Polymerase chain reaction
Genome
Breast Neoplasms
Cell Line
Polymerase Chain Reaction
Acids
Conformations

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

Trapping of genes induced upon growth arrest after treatment with antiestrogen or retinoids using retroviral promoter trap. / Paik, Soonmyoung; Zwiebel, James A.; Lippman, Marc E.

In: Journal of Cellular Biochemistry, Vol. 53, No. S17G, 1993, p. 254.

Research output: Contribution to journalArticle

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