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Mechanism of and requirement for estrogen-regulated MYB expression in estrogen-receptor-positive breast cancer cells.

Mechanism of and requirement for estrogen-regulated MYB expression in estrogen-receptor-positive breast cancer cells. Research Abstract Details 

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  • Mechanism of and requirement for estrogen-regulated MYB expression in estrogen-receptor-positive breast cancer cells. Abstract Text:

    yvette drabschYvette Drabsch,honor hugoHonor Hugo,rui zhangRui Zhang,dennis h dowhanDennis H Dowhan,yu rebecca miaoYu Rebecca Miao,alan m gewirtzAlan M Gewirtz,simon c barrySimon C Barry,robert g ramsayRobert G Ramsay,thomas j gondaThomas J Gonda,yvette drabschYvette Drabsch,honor hugoHonor Hugo,rui zhangRui Zhang,dennis h dowhanDennis H Dowhan,yu rebecca miaoYu Rebecca Miao,alan m gewirtzAlan M Gewirtz,simon c barrySimon C Barry,robert g ramsayRobert G Ramsay,thomas j gondaThomas J Gonda,

    MYB (the human ortholog of c-myb) is expressed in a high proportion of human breast tumors, and that expression correlates strongly with estrogen receptor (ER) positivity. This may reflect the fact that MYB is a target of estrogen/ER signaling. Because in many cases MYB expression appears to be regulated by transcriptional attenuation or pausing in the first intron, we first investigated whether this mechanism was involved in estrogen/ER modulation of MYB. We found that this was the case and that estrogen acted directly to relieve attenuation due to sequences within the first intron, specifically, a region potentially capable of forming a stem-loop structure in the transcript and an adjacent poly(dT) tract. Secondly, given the involvement of MYB in hematopoietic and colon tumors, we also asked whether MYB was required for the proliferation of breast cancer cells. We found that proliferation of ER(+) but not ER(-) breast cancer cell lines was inhibited when MYB expression was suppressed by using either antisense oligonucleotides or RNA interference. Our results show that MYB is an effector of estrogen/ER signaling and provide demonstration of a functional role of MYB in breast cancer.

    Mechanism of and requirement for estrogen-regulated MYB expression in estrogen-receptor-positive breast cancer cells. Publishing Authors By Initials

    y drabschY Drabsch,h hugoH Hugo,r zhangR Zhang,dh dowhanDH Dowhan,yr miaoYR Miao,am gewirtzAM Gewirtz,sc barrySC Barry,rg ramsayRG Ramsay,tj gondaTJ Gonda,y drabschY Drabsch,h hugoH Hugo,r zhangR Zhang,dh dowhanDH Dowhan,yr miaoYR Miao,am gewirtzAM Gewirtz,sc barrySC Barry,rg ramsayRG Ramsay,tj gondaTJ Gonda,

    For similar genetic processes: gene expression: transcription, genetic research abstracts see: genetic processes: gene expression: transcription, genetic research

    PUBMED ID PMID:

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    Mechanism of and requirement for estrogen-regulated MYB expression in estrogen-receptor-positive breast cancer cells. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Proceedings of the National Academy of Sciences of

    VOLUME: 104

    Page Numbers: 13762-7

    Journal Abbreviation: Proc. Natl. Acad. Sci. U.S.A.

    ISSN: 0027-8424

    DAY: 9

    MONTH: 08

    YEAR: 2007

    Mechanism of and requirement for estrogen-regulated MYB expression in estrogen-receptor-positive breast cancer cells. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 7505876

    Mechanism of and requirement for estrogen-regulated MYB expression in estrogen-receptor-positive breast cancer cells. Keywords Mesh Terms:

    KEYWORDS: Transcription, Genetic

    MESH TERMS: genetics

    Chemical & Substance for Abstract: Mechanism of and requirement for estrogen-regulated MYB expression in estrogen-receptor-positive breast cancer cells. Information

    Substance Name: Receptors, Estrogen

    Registry Number: 0

    Grant and Affiliation Information for Mechanism of and requirement for estrogen-regulated MYB expression in estrogen-receptor-positive breast cancer cells.

    AFFILIATION: University of Queensland Diamantina Institute for Cancer, Immunology, and Metabolic Medicine, Brisbane, Queensland 4102, Australia.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NCI

    GRANT: R01-CA101859

    ACRONYM: CA

    MEDLINETA: Proc Natl Acad Sci U S A

    REFSOURCE:

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