Unknown,Transcriptomics,Genomics,Proteomics

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Gene expression profiles elicited by estradiol and endoxifen in MCF7 parental and ER-beta expressing breast cancer cells


ABSTRACT: We have previously demonstrated that endoxifen is the most important tamoxifen metabolite responsible for eliciting the anti-estrogenic effects of this drug in breast cancer cells expressing estrogen receptor-alpha. However, the relevance of estrogen receptor-beta in mediating endoxifen action has yet to be explored. Therefore, the goals of this study were to determine the differences in the global gene expression profiles elicited by estradiol treatment and endoxifen between parental MCF7 breast cancer cells (expressing estrogen receptor alpha only) and MCF7 cells stably expressing estrogen receptor beta. Total RNA was isolated from parental or estrogen-receptor beta expressing MCF7 cells following 24 hour treatments with either ethanol vehicle, 1nM 17-beta-estradiol or 1nM estradiol plus 40nM endoxifen. All studies were conducted in biological replicates of 2.

ORGANISM(S): Homo sapiens

SUBMITTER: John Hawse 

PROVIDER: E-GEOD-27375 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Estrogen receptor-beta sensitizes breast cancer cells to the anti-estrogenic actions of endoxifen.

Wu Xianglin X   Subramaniam Malayannan M   Grygo Sarah B SB   Sun Zhifu Z   Negron Vivian V   Lingle Wilma L WL   Goetz Matthew P MP   Ingle James N JN   Spelsberg Thomas C TC   Hawse John R JR  

Breast cancer research : BCR 20110310 2


<h4>Introduction</h4>We have previously demonstrated that endoxifen is the most important tamoxifen metabolite responsible for eliciting the anti-estrogenic effects of this drug in breast cancer cells expressing estrogen receptor-alpha (ERα). However, the relevance of ERβ in mediating endoxifen action has yet to be explored. Here, we characterize the molecular actions of endoxifen in breast cancer cells expressing ERβ and examine its effectiveness as an anti-estrogenic agent in these cell lines.  ...[more]

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