RNA-sequencing and MeDIP-sequencing of shSRC-1 and shNT tamoxifen treated LY2 cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA389208 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5644200_1.fastq.gz | Fastqsanger.gz | |||
| SRR5644200_2.fastq.gz | Fastqsanger.gz | |||
| SRR5644201_1.fastq.gz | Fastqsanger.gz | |||
| SRR5644201_2.fastq.gz | Fastqsanger.gz | |||
| SRR5644202_1.fastq.gz | Fastqsanger.gz |
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Project description:MeDIP-sequencing of shSRC-1 and shNT tamoxifen treated LY2 cells
| PRJNA389215 | ENA
Project description:The steroid co-activator protein SRC-1 plays an important role in endocrine therapy resistant breast cancer. Its expression is associated with large high grade tumours, HER2 positivity, disease recurrence and resistance to endocrine therapy. While SRC-1 typically functions to activate gene expression, some evidence has pointed towards a potential role in repression. This study looks into the effects of a stable knockdown of SRC-1 in a tamoxifen resistant cell line, LY2, and the effects of this knock down on the methylation landscape.
2018-06-04 | GSE99648 | GEO
Project description:RNA-sequencing of shSRC-1 and shNT tamoxifen treated LY2 cells
| PRJNA389214 | ENA
Project description:SRC-1 (NCOA1) is a steroid receptor coactivator that has been associated with various aspects of the progression of breast cancer disease such as tamoxifen resistance, metastasis, cell proliferation and invasiveness. In a tamoxifen resistant breast cancer cell line (LY2), SRC-1 has been found to interact with the developmental transcription factor HoxC11. ChIP-sequencing of HoxC11 in LY2 cells shows where the transcription factor binds throughout the genome. LY2 cells were treated with either tamoxifen or vehicle and immunoprecipitated with anti-Hoxc11
2014-01-14 | E-GEOD-54027 | biostudies-arrayexpress
Project description:Introduction: Although changes in microRNA (miRNA) expression correlate with breast cancer diagnostic markers, comparatively little is known about miRNA regulation by selective estrogen receptor modulators (SERMs), e.g., tamoxifen (TAM), or their role in endocrine-resistance. Methods: A microarray approach was used to identify miRNAs differentially expressed and regulated by 4-hydroxyTAM (4-OHT) in MCF-7/TAM-sensitive versus LY2 TAM/endocrine-resistant human breast cancer cells after 6 h treatment. The expression of specific miRNAs was validated by quantitative, real-time PCR. Control miRNAs and time-course studies showed important gene-, time-, and cell- specific differences in miRNA expression. Results: 97 miRNAs were differentially expressed in MCF-7 versus LY2 cells. Bioinformatic analyses to impute the biological significance of these miRNAs by identifying 36 predicted gene targets of these miRNAs from amongst those reported to be regulated by MCF-7 cells was performed and agreement was found in direction of anticipated regulation for 12 of those putative targets. Among the miRNAs differentially expressed in MCF-7 versus LY2 cells, and that putatively target mRNAs regulated by 4-OHT in MCF-7 cells, are: miRs- 10a, 21, 22, 29a, 93, 125b, 181, 200a, 200b, 200c; 205, 221, and 222. Q-PCR assessment showed agreement with microarray data: miR- 10a, 22, 125b, 181, and 222 are higher in LY2 whereas miR-21 and miR-200a are lower in LY2 than MCF-7. 4-OHT increased miR-10a, miR-21, miR-22, miR-125b, miR-181a, miR-200a, and miR-222 in MCF-7 cells and reduced miR-10a in LY2 cells. E2 reduced the miR-21expression in MCF-7 cells. Treatment with ICI 182,780 revealed that ER suppresses miR-10a, miR-21, miR-22, miR-200a, miR-221, and miR-222 expression in MCF-7 cells. Time-dependent changes in select miRNA expression were observed in control, E2, and 4-OHT-treated MCF-7 cells. ESR1/ERα was significantly lower in LY2 than MCF-7, commensurate with higher let-7 family member, miR-221, and miR-222 expression in LY2. Reflecting inverse association with miR-200 family expression, the expression of ZEB1 was higher in LY2 than MCF-7 cells and concomitantly, E-cadherin expression was absent in LY2 cells indicating that LY2 have undergone epithelial to mesenchymal transition. Conclusions: Our studies identifying miRNAs with opposite expression between the two cell lines, indicate the involvement of these miRNAs in endocrine resistance.
2011-03-30 | GSE28267 | GEO
Project description:To assess the global effects of HOXC11 in endocrine resistant breast cancer cells we performed RNA-seq on LY2 cells which were transfected with either siRNA targeting HOXC11 (siHOXC11) or a scrambled negative control siRNA (scrHOXC11) in the presence of 4-OH-tamoxifen (10-8M). Knockdown was verified by Taq-man qRT-PCR prior to library preparation. RNA (10µg) was extracted using an Oligotex mRNA kit (Qiagen) as per manufacturer’s instructions (n=4). RNA was reverse transcribed followed by mRNA library preparation and sequencing based on a protocol outlined by Wilhelm et al., 2010. Sequencing was performed on an Illumina Genome Analyzer II (GAII) (54 million reads per sample on average).
2016-07-11 | GSE71139 | GEO
Project description:Introduction: Although changes in microRNA (miRNA) expression correlate with breast cancer diagnostic markers, comparatively little is known about miRNA regulation by selective estrogen receptor modulators (SERMs), e.g., tamoxifen (TAM), or their role in endocrine-resistance. Methods: A microarray approach was used to identify miRNAs differentially expressed and regulated by 4-hydroxyTAM (4-OHT) in MCF-7/TAM-sensitive versus LY2 TAM/endocrine-resistant human breast cancer cells after 6 h treatment. The expression of specific miRNAs was validated by quantitative, real-time PCR. Control miRNAs and time-course studies showed important gene-, time-, and cell- specific differences in miRNA expression. Results: 97 miRNAs were differentially expressed in MCF-7 versus LY2 cells. Bioinformatic analyses to impute the biological significance of these miRNAs by identifying 36 predicted gene targets of these miRNAs from amongst those reported to be regulated by MCF-7 cells was performed and agreement was found in direction of anticipated regulation for 12 of those putative targets. Among the miRNAs differentially expressed in MCF-7 versus LY2 cells, and that putatively target mRNAs regulated by 4-OHT in MCF-7 cells, are: miRs- 10a, 21, 22, 29a, 93, 125b, 181, 200a, 200b, 200c; 205, 221, and 222. Q-PCR assessment showed agreement with microarray data: miR- 10a, 22, 125b, 181, and 222 are higher in LY2 whereas miR-21 and miR-200a are lower in LY2 than MCF-7. 4-OHT increased miR-10a, miR-21, miR-22, miR-125b, miR-181a, miR-200a, and miR-222 in MCF-7 cells and reduced miR-10a in LY2 cells. E2 reduced the miR-21expression in MCF-7 cells. Treatment with ICI 182,780 revealed that ER suppresses miR-10a, miR-21, miR-22, miR-200a, miR-221, and miR-222 expression in MCF-7 cells. Time-dependent changes in select miRNA expression were observed in control, E2, and 4-OHT-treated MCF-7 cells. ESR1/ER? was significantly lower in LY2 than MCF-7, commensurate with higher let-7 family member, miR-221, and miR-222 expression in LY2. Reflecting inverse association with miR-200 family expression, the expression of ZEB1 was higher in LY2 than MCF-7 cells and concomitantly, E-cadherin expression was absent in LY2 cells indicating that LY2 have undergone epithelial to mesenchymal transition. Conclusions: Our studies identifying miRNAs with opposite expression between the two cell lines, indicate the involvement of these miRNAs in endocrine resistance. The purpose of this experiment is: 1. To identify miRNAs that are regulated (up or down) by 4-OHT in MCF-7 and LY2 cell lines (comparison of values from EtOH versus 4-OHT treated cells). 2. To identify miRNAs that are differentially regulated under basal (EtOH) conditions between MCF-7 and LY2 cell lines. 3. To identify miRNAs that are differentially regulated by 4-OHT in MCF-7 versus LY2 cells.
2011-03-30 | E-GEOD-28267 | biostudies-arrayexpress
Project description:Tamoxifen enhances romidepsin-induced senescence in pancreatic cancer cells. We compared gene-expression profile among untreated control, romidepsin-treated, tamoxifen-treated, and romidepsin plus tamoxifen-treated Panc1 cells.
2021-08-21 | GSE182526 | GEO
Project description:The steroid co-activator protein SRC-1 plays an important role in endocrine therapy resistant breast cancer. Its expression is associated with large high grade tumours, HER2 positivity, disease recurrence and resistance to endocrine therapy. SRC-1's role in affecting the transcriptome of the breast cancer endocrine resistant setting is uncovered through this RNA-seq analysis of LY2 cells grown with or without the presence of SRC-1
2018-06-04 | GSE99647 | GEO
Project description:SRC-1 (NCOA1) is a steroid receptor coactivator that has been associated with various aspects of the progression of breast cancer disease such as tamoxifen resistance, metastasis, cell proliferation and invasiveness. In a tamoxifen resistant breast cancer cell line (LY2), SRC-1 has been found to interact with the developmental transcription factor HoxC11. ChIP-sequencing of HoxC11 in LY2 cells shows where the transcription factor binds throughout the genome.
2014-01-14 | GSE54027 | GEO