HR+/HER2- Breast Cancer Cell and Normal Breast Epithelial Cell Derived Exosome RNA Expression
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ABSTRACT:
PROVIDER: PRJNA854659 | ENA |
REPOSITORIES: ENA
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Project description:AS a key medium for intercellular communication, exosome plays an important role in the occurrence and development of various forms of cancers, including breast cancer. However, the RNA from breast cancer-derived exosome remains to be explored. The HR+/HER2− breast cancer is the most common subgroup of breast cancer, we collected and primary cultured breast cancer and normal breast epithelial cells from three HR+/HER2− breast cancer patients, isolated the supernatant and extracted RNA from exosomes, and then performed microarray assays.
2023-10-01 | GSE207304 | GEO
Project description:Hormone receptor-positive (HR+)/human epidermal growth factor receptor 2-negative (HER2-) breast cancer, the most common type of breast cancer, is facing challenges such as endocrine therapy resistance and distant relapse. Immunotherapy has shown progress in treating triple-negative breast cancer, but immunological research on HR+/HER2- breast cancer is still in its early stages. Here, we performed a multi-omics analysis of a large cohort of HR+/HER2- breast cancer patients (n = 351) and revealed that HR+/HER2- breast cancer possessed a highly heterogeneous tumor immune microenvironment. Notably, the immunological heterogeneity of HR+/HER2- breast cancer was related to MAP3K1 mutation and we validated experimentally that MAP3K1 mutation could attenuate CD8+ T cell-mediated antitumor immunity. Mechanistically, MAP3K1 mutation suppressed MHC-I-mediated tumor antigen presentation through promoting the degradation of antigen peptide transporter 1/2 (TAP1/2) mRNAs, thereby driving tumor immune escape. In preclinical models, the postbiotics tyramine could reverse the MAP3K1 mutation-induced MHC-I reduction, thereby augmenting the efficacy of immunotherapy.
2024-12-20 | GSE276527 | GEO
Project description:Breast cancer, categorised into hormone receptor-positive (HR+), HER2-positive (HER2+), and triple-negative (TNBC) subtypes, exhibits varied outcomes based on the number of tumour-infiltrating lymphocytes (TILs). Increased TIL levels are associated with better outcomes in HER2+ and TNBC, while HR+ individuals with high TIL levels show shorter survival but greater neoadjuvant chemotherapy response. To explore the divergent roles of TIL levels across various subtypes and their effect on immune cell composition, we employed single-cell RNA sequencing on 31 patients with breast cancer. HR+ breast cancer with high TIL levels (TIL-high) revealed increased SPP1+ macrophages, increased SPP1 expression in other monocytes/macrophages (mono/macro) subgroups, and enriched pathways associated with extracellular matrix (ECM) remodelling in mono/macro. Moreover, cell–cell interaction analyses revealed enhanced SPP1, MIF, and FN1 signalling in the interaction between SPP1+ macrophages and T-cells in TIL-high HR+ breast cancer. Spatial transcriptomics data highlighted the close proximity of SPP1+ macrophages, CD8+ T-cells, and CD4+ T-cells in TIL-high HR+ breast cancer. Our findings unveil the novel influence of SPP1+ macrophages on T-cells in TIL-high HR+ breast cancer, potentially explaining the poor prognosis and offering insights for targeted interventions.
2024-10-09 | GSE261774 | GEO
Project description:We established an acquired trastuzumab-resistant model in vitro from a trastuzumab-sensitive, HER2-amplified breast-cancer cell line. A multi-omic strategy was implemented to obtain gene, proteome, and phosphoproteome signatures associated with acquired resistance to trastuzumab in HER2-positive breast cancer, followed by validation in human clinical samples.
2020-06-01 | PXD010574 | Pride
Project description:Comparison of matched cfDNA and CTC gDNA in HR+HER2- metastatic breast cancer patients
| PRJEB33921 | ENA
Project description:The high incidence of the HR+/HER2- breast cancer subtype is a major public health concern, leading us to explore the way three arms of the tumor microenvironment (TME) – hormonal, inflammatory and growth-stimulating – affect tumor progression in this disease. Our past findings indicate that such a joint “TME Stimulation” induces pro-metastatic traits in HR+/HER2- cells, primarily enrichment of cancer stem cells (CSCs), playing key roles in metastasis in vivo. Here, we reveal unexpected roles for STAT3 in this setting, serving as negative regulator that limits CSC enrichment while promoting cancer cell abilities to exploit the immune/inflammatory system in their favor. Moreover, our data provide evidence to novel roles for the strong pro-inflammatory transcription factor p65, whose activities could compensate for complete loss of STAT3 and recapitulate its ability to limit CSC enrichment. These findings call for in depth studies on STAT3 and p65 roles in regulating TME activities in malignant diseases.
2023-04-19 | GSE226339 | GEO
Project description:Expression data from HER2+ breast cancer cell lines.
| PRJNA812395 | ENA
Project description:In the normal breast, PMCA2 transports calcium into milk. It is also upregulated in breast cancer cells and high tumor levels predict increased mortality in patients. In this study, we examined interactions between PMCA2 and HER2. We find that PMCA2 and a scaffolding protein, NHERF1, interact together with HER2 in specific membrane domains protruding from the surface of breast cancer cells. Knocking down PMCA2 or NHERF1 increases intracellular calcium and leads to the ubiquitination, endocytosis and degradation of HER2 after receptor activation. This is associated with reductions in HER2 expression and signaling. Manipulating PMCA2 levels regulates proliferation and apoptosis of breast cancer cells in vitro and knocking out PMCA2 dramatically inhibits the formation of hyperplasia and tumors in MMTV-Neu mice. Gene expression profiling was performed on control SKBR3 cells vs. PMCA2, NHERFR1 and HER2 knock down cells. Each group has 6 duplicates.
2014-10-22 | E-GEOD-62555 | biostudies-arrayexpress
Project description:In the normal breast, PMCA2 transports calcium into milk. It is also upregulated in breast cancer cells and high tumor levels predict increased mortality in patients. In this study, we examined interactions between PMCA2 and HER2. We find that PMCA2 and a scaffolding protein, NHERF1, interact together with HER2 in specific membrane domains protruding from the surface of breast cancer cells. Knocking down PMCA2 or NHERF1 increases intracellular calcium and leads to the ubiquitination, endocytosis and degradation of HER2 after receptor activation. This is associated with reductions in HER2 expression and signaling. Manipulating PMCA2 levels regulates proliferation and apoptosis of breast cancer cells in vitro and knocking out PMCA2 dramatically inhibits the formation of hyperplasia and tumors in MMTV-Neu mice.
2014-10-22 | GSE62555 | GEO
Project description:HER2-positive (HER2+) breast cancer patients that do not respond to targeted treatment have a poor prognosis. The effects of targeted treatment on endogenous microRNA (miRNA) expression levels are unclear. We report that responsive HER2+ breast cancer cell lines had a higher number of miRNAs with altered expression after treatment with trastuzumab and lapatinib compared to poorly responsive cell lines. To evaluate whether miRNAs can sensitize HER2+ cells to treatment, we performed a high-throughput screen of 1626 miRNA mimics and inhibitors in combination with trastuzumab and lapatinib in HER2+ breast cancer cells. We identified eight miRNA mimics sensitizing cells to targeted treatment, miR-101-5p, mir-518a-5p, miR-19b-2-5p, miR-1237-3p, miR-29a-3p, miR-29c-3p, miR-106a-5p, and miR-744-3p. A higher expression of miR-101-5p predicted better prognosis in patients with HER2+ breast cancer (OS: p=0.0392; BCSS: p=0.0125), supporting the tumor-suppressing role of this miRNA. In conclusion, we have identified miRNAs that sensitize HER2+ breast cancer cells to targeted therapy. This indicates the potential of combining targeted drugs with miRNAs to improve current treatments for HER2+ breast cancers.
2021-05-21 | GSE163490 | GEO