Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA260379 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The mechanisms that allow breast cancer cells to metabolically sustain growth are poorly understood. In breast cancer, FoxA1 transcription factor, along with estrogen receptor, regulates luminal cell specification and proliferation. Here we report that FoxA transcription factor family members FoxA1 and FoxA2 fuel cellular growth in breast cancer through the expression of a common target gene, namely the endothelial lipase (LIPG) We used microarrays to detail the genes that are under de control of FoxA transcription factors in MDA231 and MCF7 breast cancer cells
2016-04-08 | GSE61164 | GEO
Project description:Lipid metabolism genes in contralateral unaffected breast and estrogen receptor status of breast cancer
| PRJNA177679 | ENA
Project description:Lipid uptake occurs through caveolae, plasma membrane invaginations formed by caveolins (CAV) and caveolae-associated protein 1 (CAVIN1). Genetic alterations of CAV1N1 and CAV1 modify lipid metabolism and underpin lipodystrophy syndromes. Lipids contribute to tumorigenesis by providing fuel to cancer metabolism and supporting growth and signaling. Tumor stroma supports tumor proliferation, invasion and metastasis but how stromal lipids influence these processes remain to be defined. Here we show that stromal CAVIN1 regulates lipid abundance in the prostate cancer microenvironment and suppresses metastasis. We show that depletion of CAVIN1 in prostate stromal cells markedly reduces their lipid droplet accumulation and increases inflammation.
2022-01-19 | GSE146229 | GEO
Project description:Carcinoma-associated fibroblasts (CAFs) consist of heterogeneous subpopulations and play a critical role in the dynamics of the tumor microenvironment. Previously, the extracellular signals of CAFs have been attributed to extracellular matrix, cytokine, cell-surface checkpoints and exosome. Here, we showed that CD10, which is a transmembrane hydrolase expressed on a subset of CAFs, supports tumor stemness and induced chemoresistance. Mechanistically, CD10 degenerates an anti-tumoral peptide, osteogenic growth peptide (OGP). OGP restrains the expression of a rate-limiting desaturase and inhibits lipid desaturation which is required for cancer stem cells (CSCs). Therapeutically, targeting CD10 significantly improves the efficacy of chemotherapy in vivo. Clinically, CD10-OGP signals are associated with the response of neo-adjuvant chemotherapy in patients of breast cancer. Overall, our data suggested that a nexus between the niche and lipid metabolism in CSCs can be a promising therapeutic target for breast cancer.
2021-10-19 | GSE156470 | GEO
Project description:Cancer cells that seed in the lung require lipids, which are mostly produced by alveolar type II (AT2) cells. However, whether overt metastases depend on AT2 cell-derived lipids and whether AT2 cells can be targeted to reduce metastasis growth remains unknown. We discovered that metastases stimulate the proliferation of AT2 cells in their vicinity and reprogram them into lipid feeder cells in mice and patients with breast cancer using spatial mass spectrometry imaging combined with immunohistochemistry and spatial transcriptomics. Mechanistically, we find that the secretome of the metastases contains IL-6 and formate, which increase the activity of the transcription factor sterol regulatory element-binding transcription factor 1 (SREBP-1). This in turn enhances the expression of key de novo lipid synthesis genes including fatty acid synthase (FASN) and glycerol-3-phosphate acyltransferase 1 (GPAM). Deleting Fasn selectively in AT2 cells or targeting FASN and GPAM systemically is sufficient to impair breast cancer-derived metastasis growth in mice. In summary, we discovered that overt metastases reprogram AT2 cells and that targeting the lipid metabolism of AT2 cells impairs metastasis growth.
2026-02-10 | GSE318532 | GEO
Project description:FoxA transcription factors are involved in development and tumorigenesis of the gastrointestinal tract. However, the downstream programs controlled by FoxA factors remain poorly understood. The goal of this study is to understand the transcriptional responses regulated by FoxA proteins in liver and colon cancer cells. Human liver cancer cell line HepG2 and colon cancer cell line LS174T infected with lentivirus expressing shRNAs targeting human FoxA1 and FoxA2.
2013-08-01 | E-GEOD-46466 | biostudies-arrayexpress
Project description:Androgen receptor (AR) is expressed in 60-70% of breast cancers independent of estrogen receptor (ER) expression, however its function in breast cancer is largely unknown. Our study identified the high level of AR in ERâ/HER2+ breast tumors and andorgen and AR greatly stimulated growth of MDA-MB-453 breast cancer cells. To define the genome-wide AR binding sites, we performed AR ChIP-seq using MDA-MB-453 breast cancer cells followig stimulation of DHT. We also identified FOXA1 is a crucial AR cofactor in MDA-MB-453 cells and the FOXA cistrome showed signaficant overlap with AR at both early and late time points of DHT stimulation.
2011-07-11 | GSE28788 | GEO
Project description:How histone lysine crotonylation (Kcr) is read and interpreted remains to be elucidated. We report here that YEATS4, a potential breast cancer driver identified recently by two independent genome-wide association studies, is a reader of H3K14cr. Integrative metabolomic, epigenomic, and transcriptomic analyses reveal that H3K14cr reading by YEATS4 is associated with a shift of cellular metabolic profile and transcription activation of a cohort of genes, including CD36, CPT1A, and ACOX1, that are critically involved in the uptake and metabolism of fatty acids. High expression of YEATS4 fortifies fatty acid metabolism, enhances self-renewal and growth of ALDH+ breast cancer stem cells, and is correlated with poor prognosis of breast cancer patients, especially the ER+ subtype. Our work uncovers YEATS4 as an “amplifier” in the feedforward circuit of histone crotonylation and lipid metabolism underlying the stemness and cell proliferation, supporting the pursuit of YEATS4 as a potential target for breast cancer intervention.
2025-09-14 | GSE256112 | GEO
Project description:How histone lysine crotonylation (Kcr) is read and interpreted remains to be elucidated. We report here that YEATS4, a potential breast cancer driver identified recently by two independent genome-wide association studies, is a reader of H3K14cr. Integrative metabolomic, epigenomic, and transcriptomic analyses reveal that H3K14cr reading by YEATS4 is associated with a shift of cellular metabolic profile and transcription activation of a cohort of genes, including CD36, CPT1A, and ACOX1, that are critically involved in the uptake and metabolism of fatty acids. High expression of YEATS4 fortifies fatty acid metabolism, enhances self-renewal and growth of ALDH+ breast cancer stem cells, and is correlated with poor prognosis of breast cancer patients, especially the ER+ subtype. Our work uncovers YEATS4 as an “amplifier” in the feedforward circuit of histone crotonylation and lipid metabolism underlying the stemness and cell proliferation, supporting the pursuit of YEATS4 as a potential target for breast cancer intervention.
2025-09-14 | GSE256110 | GEO
Project description:Docetaxel-loaded solid lipid nanoparticles suppress breast cancer cells growth with reduced myelosuppression toxicity
| PRJNA235177 | ENA