Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcription profiling by array of human breast cancer cell line MCF7 transfected with miR221, miR222 and miR206 to identify the different functions of these microRNAs

ABSTRACT: In our previous analyses, we have identified that miR221&222 and miR206 are strongly up-regulated in Estrogen Receptor negative breast cancer cell lines and primary tumor. Moreover we have shown that miR221&222 and miR206 target the Estrogen Receptor. In order to identify the different function of miR221&222 and miR206 in breast cancer cells, an Estrogen Receptor positive breast cancer cells MCF7 was transfected with the different microRNAs and gene expression profile was carried out. We identified that miR221&222 up-modulation increase the tumorigenicity of breast cancer cells compared to miR206.

ORGANISM(S): Homo sapiens

SUBMITTER: Cristian Taccioli

PROVIDER: E-TABM-601 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

MicroRNA cluster 221-222 and estrogen receptor alpha interactions in breast cancer.

Di Leva Gianpiero G Gasparini Pierluigi P Piovan Claudia C Ngankeu Apollinaire A Garofalo Michela M Taccioli Cristian C Iorio Marilena V MV Li Meng M Volinia Stefano S Alder Hansjuerg H Nakamura Tatsuya T Nuovo Gerard G Liu Yunlong Y Nephew Kenneth P KP Croce Carlo M CM

Journal of the National Cancer Institute 20100413 10

<h4>Background</h4>Several lines of evidence have suggested that estrogen receptor alpha (ERalpha)-negative breast tumors, which are highly aggressive and nonresponsive to hormonal therapy, arise from ERalpha-positive precursors through different molecular pathways. Because microRNAs (miRNAs) modulate gene expression, we hypothesized that they may have a role in ER-negative tumor formation.<h4>Methods</h4>Gene expression profiles were used to highlight the global changes induced by miRNA modulat ...[more]

PMID: 20388878

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Project description:Estrogen receptor positive breast cancer is the most prevalent form of breast cancer. Although a number of available drugs are highly effective at blocking estrogen mediated receptor activity, thousands of patients die every year from ER positive breast cancers because the disease progresses to a stage at which these drugs are no longer effective. Thus, it is crucial to establish a comprehensive understanding of the biology of the estrogen receptor (ER) in ER:positive breast cancers that progress despite hormone therapy, a gap in knowledge that remains a serious impediment to successful treatment of patients with ER positive breast cancer. A key question that must be answered is how the estrogen receptor retains the capacity to activate transcription in the absence or near absence of estrogen. We have found a partial answer to this question upon investigating the effect of amplification and overexpression of Wolf Hirschhorn Syndrome Candidate 1:Like 1 (WHSC1L1), a gene that is amplified in 15% of breast cancers that codes for a histone:lysine methyltransferase. WHSC1L1 lies in the 8p11:p12 amplicon, a region of gene amplification that is strongly associated with breast cancer. In this study, we performed shRNA knockdown of the catalytically inactive short isoform of WHSC1L1 in SUM44PE breast cancer cells and found that expression of the short isoform of WHSC1L1 is necessary for expression of the estrogen receptor in this highly ER:positive cell line. In addition, we found that the estrogen receptor binds chromatin extensively in the absence of exogenous estrogen, including several actively transcribed canonical ER target genes, indicating that estrogen receptor signaling is active in SUM44 cells in estrogen free conditions. These findings represent a novel model for ER biology in luminal B breast cancers harboring amplification of WHSC1L1 and provide insight into the mechanisms by which ER: positive breast cancers become unresponsive to SERMs or aromatase inhibitors.

Dataset Information

Transcription profiling by array of human breast cancer cell line MCF7 transfected with miR221, miR222 and miR206 to identify the different functions of these microRNAs

Publications

MicroRNA cluster 221-222 and estrogen receptor alpha interactions in breast cancer.

Similar Datasets

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