Transcriptome profiling of ER+ breast cancer primary tumor and its tumorsphere derivative
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE84054 | GEO | 2017/09/24
SECONDARY ACCESSION(S): PRJNA327871
REPOSITORIES: GEO
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Project description:<p>These are tumor biopsies and corresponding normal samples from patients with early stage ER+/HER2- breast cancer who had received the aromatase inhibitor letrozole for 10-21 days prior to surgery.</p>
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Project description:We performed single cell RNA sequencing (RNA-seq) for 549 primary breast cancer cells and lymph node metastases from 11 patients with distinct molecular subtypes (BC01-BC02, estrogen receptor positive (ER+); BC03, double positive (ER+ and HER2+); BC03LN, lymph node metastasis of BC03; BC04-BC06, human epidermal growth factor receptor 2 positive (HER2+); BC07-BC11, triple-negative breast cancer (TNBC); BC07LN, lymph node metastasis of BC07) and matched bulk tumors. We separated these single cells into epithelial tumor and tumor-infiltrating immune cells using inferred CNVs from RNA-seq. The refined single cell profiles for the tumor and immune cells provide key expression signatures of breast cancer and the surrounding microenvironment.
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Project description:Purpose: To investigate the critical role ER stress exhibit in cellular crosstalk between tumor cells and macrophages in the tumor microenvironment. We performed the two different polarized macrophages under ER stress and harvested the ER-stressed conditioned media. To figure out how two macrophage polarities generated conditioned media impact LLC tumor cells diversely, we use RNA-sequencing (RNA-seq) strategies to profile the deep-sequencing research and find the potential molecular mechanisms during the ER stress transmission from macrophages to tumor cells. The major differential influences the two macrophages proceeded were attribute to macrophages polarization characteristics, which instruct us to study the two polarized macrophages. Hence, we also performed RNA-sequencing during in vitro stimulation of ER stress inducer Tm in two polarized bone marrow derived macrophages. Methods: After different treatment, LLC tumor cells mRNA was extracted and LLC tumor cells transcriptome profiles were generated by deep sequencing, using Illumina. Under ER stress, the different polarized macrophages transcriptome profiles were also generated by deep sequencing, using Illumina. Results: Macrophages displayed different polarization characteristics could respond to ER stress differentially. Notably, GM-BMDMs were more susceptible to ER stress and facilitated the induction of proinflammatory signals, and M-BMDMs facilitate tumor growth, process, and metastasis. LLC cells exhibit different gene expression profiles in response to transferred ER stress from two polarized macrophage populations. Tumor cells that received transmissible ER stress from M2 macrophages has potential to facilitate the tumor survival, while transmissible ER stress from M1 macrophages could lead to more acute cell death and inflammation. Conclusion: Our study revealed that tumor cells could receive the transmissible ER stress from distinct macrophage populations with different extents of ER stress activation in the tumor microenvironment. The proinflammatory M1-like macrophages respond to ER stress more potently and transmit stronger ER stress to tumor cells. By analyzing the secreted components of two ER stressed macrophage populations, we identified that S100A8 and S100A9, which are dominantly secreted by M1-like macrophages, could lead to significant recipient tumor cell death in synergy with transferred ER stress.
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Project description:Estrogen receptor (ER) signaling–dependent cancer cell growth is one of the major features of ER-positive breast cancer (BC). Inhibition of ER function is a standard and effective treatment for ER-positive tumors; however, ~20% of patients with ER-positive BC experience early or late recurrence. In this study, we examined intertumor heterogeneity from an epigenetic perspective based on the hypothesis that the intrinsic difference in epigenetic states around ER signaling pathway underlies endocrine therapy resistance. We profiled chromatin accessibility data from 42 BC samples, including 35 ER-positive human epidermal growth factor receptor 2 (HER2)-negative and 7 triple-negative tumors, identifying a subgroup of ER-positive BCs with a distinctive chromatin accessibility pattern including reduced accessibility to ER-responsive elements (EREs). The same subgroup was also observed in The Cancer Genome Atlas BC cohort. Despite the reduced accessibility to EREs, the expression of ER and potential ER target genes were not decreased in these tumors. Our findings highlight the existence of a subset of ER-positive BCs with unchanged ER expression but reduced EREs accessibility that cannot be distinguished by conventional immunostaining for ER. Future studies should determine whether these tumors are associated with resistance to endocrine therapy.
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Project description:The objective of this study was to determine the extent to which paracrine action of 17-beta-estradiol on ER+ mouse astrocytes, affect gene expression of MDA231-derived brain trophic 231BR cells.
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Project description:G0/G1 switch gene 2 (G0S2) is known to inhibit lipolysis through inhibition of adipose triglyceride lipase (ATGL). Although G0S2 has also been proposed to be involved in cancer progression, this role appears complex, and mechanisms are unclear. We recently reported a role for G0S2 in ER+ breast cancer suppression as low G0S2 expression correlated with increased recurrence after antiestrogen therapy and increased G0S2 expression sensitized ER+ breast cancer cells to tamoxifen and PI3K/mTOR inhibitors. In this report we dissect the role of G0S2 in ER+ versus ER- breast cancer. Overexpression of G0S2 in ER- breast cancer cells increased cell proliferation while G0S2 overexpression in ER+ breast cancer cells decreased cell proliferation. Transcriptome analysis revealed that G0S2 mediated distinct but overlapping transcriptional responses in ER- and ER+ cells. G0S2 reduced genes associated with an epithelial phenotype, especially in ER- cells, including CDH1, ELF3, STEAP4 and TACSTD2 suggesting promotion of the epithelial-mesenchymal transition (EMT). G0S2 also repressed estrogen signaling and estrogen receptor target gene signatures, especially in ER+ cells, including TFF1 and TFF3. In addition, G0S2 overexpression increased cell migration in ER- cells and increased estrogen deprivation sensitivity in ER+ cells. Interestingly, two genes downstream of ATGL in fat utilization, HMGCS1 and HMGCS2, that are also rate-limiting in steroid hormone biosynthesis, were downregulated in G0S2 overexpressing ER+ cells. In addition, HSD17B11, a gene that converts estradiol to its less estrogenic derivative, estrone, was highly upregulated in G0S2 overexpressing ER+ cells, suggesting G0S2 overexpression has a negative effect of estradiol production and maintenance. High levels of estrone were confirmed to be present in G0S2 overexpressing cells. High expression of G0S2 and HSD17B11 was associated with improved relapse free survival in breast cancer patients while high expression of HMGSC1 was associated with poor survival. In addition, the expression of G0S2 positively and negatively correlated respectively, with expression of HSD17B11 and HMGSC1 in patient samples. Finally, we deleted G0S2 in breast cancer prone MMTV-PyMT mice that have been hypothesized to be partially estrogen sensitive during early stages of tumorigenesis but develop ER- tumors. In this context, G0S2 functioned as a tumor promoter, with G0S2 null mice demonstrating a slight increase in tumor latency and decrease in tumor weight and a larger inhibitory effect on tumor metastasis. Our data indicates a complex role for G0S2 in breast cancer, dependent on ER status, that may be mediated in part by suppression of the estrogen signaling pathway.
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