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Major impact of sampling methodology on gene expression in estrogen receptor positive breast cancer

ABSTRACT: Major impact of sampling methodology on gene expression in estrogen receptor positive breast cancer

PROVIDER: PRJNA415551 | ENA |

REPOSITORIES: ENA

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Major impact of sampling methodology on gene expression in estrogen receptor positive breast cancer

Project description:To investigate the impact of sampling methodology on gene expression data from primary estrogen receptor positive (ER+) breast cancer biopsies. Analysis of global gene-expression measured in core-cut biopsies at baseline and surgery from patients randomised to receive either 2-week’s presurgical aromatase inhibitor (AI, n=157) or no presurgical treatment (n=56) revealed genes most markedly altered in the AI group (e.g. FOS, DUSP1, RGS1, FOSB) were equally altered in the no-treatment group; some widely investigated genes that were apparently unaffected in the AI group (e.g. MYC) were counter-altered in the Control group masking actual AI-dependent changes. In the absence of a Control group these artefactual changes would likely lead to the most affected genes being the erroneous focus of research. The findings are likely relevant to all archival collections of ER+ breast cancer.

2018-10-22 | GSE105777 | GEO

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Project description:Comparison between Estrogen receptor positive and Estrogen receptor negative breast cancer samples Keywords: breast cancer type comparison

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Estrogen-induced lncRNA, LINC02568, promotes estrogen receptor-positive breast cancer development and drug resistance through both in trans- and in cis-mechanisms

Project description:Estrogen and estrogen receptor (ER) signaling play critical roles in the development of ER-positive breast cancer, and endocrine therapy is the frontline treatment for ER-positive breast cancer patients. However, the primary and acquired resistance to endocrine therapy including tamoxifen and fulvestrant remains as the major challenge in the clinic. Here, we identified an estrogen-induced lncRNA, LINC02568, through transcriptomic analysis, which is highly expressed in ER-positive breast cancer. LINC02568 is functional important in ER-positive breast cancer cell growth in vitro and tumorigenesis in vivo as well as endocrine therapy resistance. Mechanically, we demonstrated that LINC02568 regulates, in trans, estrogen/ERα-induced gene transcriptional activation by sponging miR-1233-5p to stabilize ESR1 mRNA in the cytoplasm. Meanwhile, LINC02568 contributes to tumor-specific pH homeostasis in breast cancer cells by regulating CA12 in cis in the nucleus. The dual functions of LINC02568 together contribute to breast cancer cell growth and tumorigenesis as well as endocrine therapy resistance. Antisense oligonucleotides (ASO) targeting LINC02568 significantly inhibits ER-positive breast cancer cell growth in vitro and tumorigenesis in vivo as well as resensitize tamoxifen-resistant cells to tamoxifen. Furthermore, combination treatment with ASO targeting LINC02568 and tamoxifen exhibits synergistic effect on tumor growth. Taken together, our findings revealed dual mechanisms of LINC02568 in regulating ERα signaling and pH homeostasis in ER-positive breast cancer, and indicated that targeting LINC02568 might represent a potential therapeutic avenue in clinic.

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2015-08-21 | PXD000484 | Pride

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