Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

High calcium inducible genes in triple negative breast cancer cells

ABSTRACT: Malignant breast cancer is often associated with skeletal metastasis and co-morbidities such as cancer-induced hypercalcemia. Although circulating calcium has been linked to aggressive and larger breast tumors, the mechanisms underlying the potential oncogenic effects of high calcium remain poorly understood. Here, we assessed the effects of high extracellular calcium on the modulation of gene expression in TNBC cells. This study showed that chronic high calcium attenuates the activity of the calcium sensing receptor but promotes the growth and migration of triple negative breast cancer cells. We also show that in TNBC cells, high extracellular calcium triggered the expression of early response genes such as FOS/FOSB and subsequently, mailgnancy assoicated genes including the cancer testis antigen MAGEC2. This study provides novel mechanistic insights into the hitherto unappreciated oncogenic effects of high extracellular calcium especially in malignant or late-stage breast cancers.

ORGANISM(S): Homo sapiens

PROVIDER: GSE189520 | GEO | 2021/11/26

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

E-GEOD-7377

Project description:Transcription profiling of human pre-malignant breast cancer samples

2025-01-24 | E-GEOD-7377 | ExpressionAtlas

E-MTAB-6120

Project description:Uncoupling effects of ERalfa on LKB1/AMPK interaction upon adiponectin exposure in breast cancer

2025-01-23 | E-MTAB-6120 | ExpressionAtlas

E-GEOD-16873

Project description:Early Dysregulation of Cell Adhesion and Extracellular Matrix Pathways in Breast Cancer Progression

2025-01-24 | E-GEOD-16873 | ExpressionAtlas

Calcium Handling in Breast Cancer

Project description:Extracellular calcium export by the breast ductal epithelium is crucial during lactation and plays a significant role in breast cancer progression. Intraductal calcium deposition is a hallmark of aggressive premalignant lesions. This study tested the hypothesis that microbiome-derived extracellular vesicles (EVs) influence calcium modulation within premalignant breast cancer lesions. Based on the analysis of plasma, serum, saliva, and tissue collected from breast cancer patients and controls (N=150), Lactobacillus rhamnosus (Lr) was chosen as the model microbiota. In a BT-474 human breast cancer cell line monolayer culture under acute calcium stress, Lr EVs enhanced intracellular calcium intake. In a BT474 3D spheroid model under chronic calcium stress, Lr EVs increased extracellular calcium deposition and the mRNA expression of calcium export channel calcium pump isoform 2 (PMCA2) and stromal interaction molecule 1 (STIM1) in a dose-dependent manner. We propose that Lr EVs influence calcium regulation and mineral deposition, thereby affecting premalignant breast cancer progression.

2025-03-11 | MSV000097290 | MassIVE

MicroRNA expression data from an epithelial-mesenchymal transition (EMT) model of triple negative breast cancer (TNBC).

Project description:Triple-negative breast cancer (TNBC) is the most aggressive form of breast cancer due to lack of effective targeted therapies. Here, we report that the expression of miR-4417 is suppressed during the progression of TNBC cells from non-malignant to the malignant stage. miR-4417 is localized to chromosome 1p36, a region with high loss of heterozygosity in multiple cancers, and its biogenesis is DICER-dependent. Low expression of miR-4417 is significantly associated with worse prognosis in TNBC patients, while overexpression of miR-4417 is sufficient to inhibit migration and tumorigenecity of TNBC cells in vitro. Overall, our findings suggest that miR-4417 exerts a tumor suppressive effect and thereby could serve as a prognostic biomarker and therapeutic tool against TNBC. We used microarrays to profile the global miRNA changes during EMT to identify putative tumor suppressors and prognostic biomarkers for TNBC.

2019-10-15 | GSE121657 | GEO

OCT-2 is associated with pro-metastatic epigenomic properties of triple-negative breast cancer cells [ChIP-seq]

Project description:Triple-negative breast cancer (TNBC) is a malignant type of breast cancer. Owing to the lack of expression of receptors that serve as molecular targets for standard therapy for breast cancer, conventional cytotoxic chemotherapy is the primary treatment option for TNBC. However, TNBC exhibits a high degree of genomic heterogeneity, rendering it resistant to chemotherapy. Therefore, there is an urgent need to identify novel therapeutic targets for the treatment of TNBC. Advances in massively parallel sequencing technology have enabled the identification of cancer cell-specific gene expression patterns and epigenetic alterations that regulate their expression. Cancer cell-specific super-enhancers (SEs) have been identified as effective therapeutic targets for cancer. In this study, we identified the functional roles of epigenetic changes and their regulatory mechanisms in TNBC cells. TNBC cell-specific SEs were formed near several genes that contribute to malignant cancer cell acquisition. We found that the transcription factor OCT-2 (encoded by POU2F2) was responsible for the formation of SEs and the expression of genes encoded in the vicinity of the SE regions. Overexpression of POU2F2 enhances the metastasis of TNBC cells in mice and their expression is highly correlated to poor prognosis of TNBC patients. Our findings provide a new insight into cancer cell-specific epigenetic changes induced by OCT-2, which trigger the progression of TNBC, and suggest possible candidates that could be targeted for the treatment of TNBC.

2025-05-14 | GSE291650 | GEO

OCT-2 is associated with pro-metastatic epigenomic properties of triple-negative breast cancer cells

2025-05-14 | GSE292004 | GEO

Identification of BBOX1 as a Therapeutic Target in Triple-Negative Breast Cancer

Project description:Triple-negative breast cancer (TNBC) is an aggressive and highly lethal disease. Because of its heterogeneity and lack of hormone receptors or HER2 expression, targeted therapy is limited. Here, by performing a functional siRNA screening for 2-OG–dependent enzymes, we identified gamma-butyrobetaine hydroxylase 1 (BBOX1) as an essential gene for TNBC tumorigenesis. BBOX1 depletion inhibits TNBC cell growth while not affecting normal breast cells. Mechanistically, BBOX1 binds with the calcium channel inositol-1,4,5-trisphosphate receptor type 3 (IP3R3) in an enzymatic-dependent manner and prevents its ubiquitination and proteasomal degradation. BBOX1 depletion suppresses IP3R3-mediated endoplasmic reticulum calcium release, therefore impairing calcium-dependent energy-generating processes including mitochondrial respiration and mTORC1-mediated glycolysis, which leads to apoptosis and impaired cell-cycle progression in TNBC cells. Therapeutically, genetic depletion or pharmacologic inhibition of BBOX1 inhibits TNBC tumor growth in vitro and in vivo. Our study highlights the importance of targeting the previously uncharacterized BBOX1–IP3R3–calcium oncogenic signaling axis in TNBC.

2020-12-02 | GSE152317 | GEO

Tubacin mediates the synthetic lethality of cysteine in breast cancer independent on HDAC6

Project description:Triple-negative breast cancer (TNBC) has a highly aggressive nature and distinct molecular characteristics from other subtypes of breast cancer and lacks effective targeted therapy. The molecular and genetic basis of cysteine/cystine dependency in TNBC is complex. We found that cysteine addiction associates with the expression of a set of Claudin genes in TNBC. The Claudin-high TNBCs are independent on cystine, while the Claudin-low TNBCs undergo rapid ferroptosis upon cystine deprivation or inhibition of cystine transport by erastin. To overcome the resistance of Claudin-high TNBC and luminal breast cancer to the potential targeted cystine-addiction therapy, we explored the synthetic lethality of cysteine by an epigenetic compound library screen. Several potent HDAC6 inhibitors were identified and rendered the Claudin-high TNBCs and luminal cancer cells dependent on extracellular cystine and undergoing ferroptosis upon cystine deprivation. The transcriptomic profiling showed that the HDAC6 inhibitor tubacin in combination with erastin activates a synthetic-lethal transcriptional program. Together, we have identified the HDAC6 inhibitors as potent therapy-sensitizers to revive the targeted cysteine-addiction therapy for various subtypes of breast cancer, not limit in the Claudin-low TNBC.

2021-06-02 | GSE154425 | GEO

Comparative Characterization of 3D Chromatin Organization in Triple-Negative Breast Cancers [ATAC-seq]

Project description:Triple-negative breast cancer (TNBC) is malignant cancer with a high risk of recurrence. To date, the underlying 3D chromatin organizations of TNBC have remained unclear. Here, using in situ Hi-C, we characterized the 3D chromatin organizations in cells representing five distinct subtypes of breast cancer (including TNBC) and TNBC tissues, compared to normal cells/tissues. We found that the global and local 3D architectures are severely disrupted in TNBC cells. Importantly, we detected CTCF-dependent TNBC-susceptible loss/gain of 3D chromatin organizations and found that these changes were strongly associated with perturbed chromatin accessibility and transcriptional dysregulations. Although some discrepancies exist between TNBC cell lines and tissues, we observed that perturbed local 3D architectures found in TNBC cells are partially conserved in TNBC tissues. Furthermore, we discovered distinct tissue-specific chromatin loops by comparing normal and TNBC tissues. Collectively, our findings provide important features of 3D chromatin organization in TNBC.

2022-05-06 | GSE167153 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data