Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA227800 | ENA |
REPOSITORIES: ENA
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Project description:Cadmium is a metalloestrogen known to activate the estrogen receptor and promote breast cancer cell growth. Previous studies have implicated cadmium in the development of more malignant tumors; however the molecular mechanisms behind this cadmium-induced malignancy remain elusive. Using clonal cell lines derived by exposing breast cancer cells to cadmium for over 6 month (MCF7-Cd4, -Cd6, -Cd7, -Cd8 and -Cd12), this study aims to identify gene expression signatures associated with chronic cadmium exposure. Our results demonstrate that prolonged exposure does not merely result in the deregulation of genes but actually leads to a distinctive expression profile. The genes deregulated in cadmium-exposed cells are involved in multiple biological processes (i.e cell growth, apoptosis, etc.) and molecular functions (i.e. cadmium/metal ion binding, transcription factor activity, etc). Hierarchical clustering demonstrates that the five clonal cadmium cell lines share a common gene expression signature of breast cancer associated genes, clearly differentiating control from cadmium exposed cells. The results presented in this study offer insights into the cellular and molecular impacts of cadmium on breast cancer carcinogenesis and emphasize the importance of studying chronic cadmium exposure as one possible mechanism of promoting breast cancer progression. To understand the effects of chronic cadmium exposure on gene expression in breast cancer, two control MCF7 parental cell lines and five different clonal cadmium-adapted cell lines (MCF7-Cd4, -Cd6, -Cd7, -Cd8, and -Cd12) - previously derived from cells chronically exposed to cadmium - were used for microarray analysis.
2013-11-16 | E-GEOD-52404 | biostudies-arrayexpress
Project description:Cadmium is a metalloestrogen known to activate the estrogen receptor and promote breast cancer cell growth. Previous studies have implicated cadmium in the development of more malignant tumors; however the molecular mechanisms behind this cadmium-induced malignancy remain elusive. Using clonal cell lines derived by exposing breast cancer cells to cadmium for over 6 month (MCF7-Cd4, -Cd6, -Cd7, -Cd8 and -Cd12), this study aims to identify gene expression signatures associated with chronic cadmium exposure. Our results demonstrate that prolonged exposure does not merely result in the deregulation of genes but actually leads to a distinctive expression profile. The genes deregulated in cadmium-exposed cells are involved in multiple biological processes (i.e cell growth, apoptosis, etc.) and molecular functions (i.e. cadmium/metal ion binding, transcription factor activity, etc). Hierarchical clustering demonstrates that the five clonal cadmium cell lines share a common gene expression signature of breast cancer associated genes, clearly differentiating control from cadmium exposed cells. The results presented in this study offer insights into the cellular and molecular impacts of cadmium on breast cancer carcinogenesis and emphasize the importance of studying chronic cadmium exposure as one possible mechanism of promoting breast cancer progression.
2013-11-16 | GSE52404 | GEO
Project description:Chronic cadmium exposure decreases the dependency of MCF7 breast cancer cells on ERα
| PRJNA554005 | ENA
Project description:To understand how chronic cadmium exposure alters the dependency of ERα in terms of gene expression, we transiently silenced ERα using ICI, an antiestrogen that promotes the degradation of ERα. MCF7 and cadmium-adapted cells (Cd7 and Cd12) were treated with ICI to mediate the degradation of ERα, and a nonbiased global gene expression analysis was conducted using RNA-seq. MCF7 shared 67.3% and 59.5% of the DE genes with Cd7 and Cd12 cells, respectively, suggesting that ERα continues to play an important role in regulating the expression of genes following chronic cadmium exposure. 138 ERE genes (76.7%) were shared by all three cell lines, in that expression changed in the same direction (either up- or downregulated). For the estrogen-responsive genes, 428 (53.6%) of the 799 genes were altered in the same direction in all three cell lines. These findings show that while a majority of ERE genes responded in the same manner to loss of ERα, more variability existed within the estrogen-responsive genes. Collectively, these results indicate that while chronic cadmium exposure leads to genome-wide transcriptional changes, ERα remains important for regulating the expression of genes and maintaining the malignant phenotypes associated with breast cancer progression.
2019-08-21 | GSE134127 | GEO
Project description:Timecourse of estradiol (10nM) exposure in MCF7 breast cancer cells.
| PRJNA106571 | ENA
Project description:Chronic Bisphenol A and Genistein Exposure in MCF7 cells
| PRJNA255108 | ENA
Project description:Chronic inflammation is a hallmark of the breast cancer tumor microenvironment and is also known to be associated with disease progression and therapeutic response. Interleukin-1 (IL-1) signaling has been widely studied in breast cancer biology; however, the long-term effect of sustained IL-1 exposure on hormone receptor–positive breast cancer cells remain poorly understood. In this study, we investigated how chronic IL-1 exposure influences inflammatory response, hormone dependency, and therapeutic sensitivity in ERα+/PR+ breast cancer models, MCF7 and T47D. Chronic IL-1 exposure attenuated response to subsequent acute IL-1 treatment, but the chronically exposed cells remained sensitive to serum deprivation, retained dependence on estrogen or progesterone receptor signaling, and responded robustly to endocrine and chemotherapeutic treatments. Extensive changes in basal gene expression and histone modification revealed that chronic IL-1 exposure alters transcriptional reprogramming and chromatin remodeling. Together, these findings demonstrate that chronic IL-1 signaling drives selective inflammatory response in hormone receptor–positive MCF7 and T47D breast cancer cells. This work underscores the continued therapeutic relevance of hormone receptor–targeted strategies in chronically inflamed tumors and provides insight into how sustained inflammatory stress shapes tumor behavior and gene regulation predicted to promote tumor progression.
2026-07-22 | GSE337025 | GEO
Project description:Chronic inflammation is a hallmark of the breast cancer tumor microenvironment and is also known to be associated with disease progression and therapeutic response. Interleukin-1 (IL-1) signaling has been widely studied in breast cancer biology; however, the long-term effect of sustained IL-1 exposure on hormone receptor–positive breast cancer cells remain poorly understood. In this study, we investigated how chronic IL-1 exposure influences inflammatory response, hormone dependency, and therapeutic sensitivity in ERα+/PR+ breast cancer models, MCF7 and T47D. Chronic IL-1 exposure attenuated response to subsequent acute IL-1 treatment, but the chronically exposed cells remained sensitive to serum deprivation, retained dependence on estrogen or progesterone receptor signaling, and responded robustly to endocrine and chemotherapeutic treatments. Extensive changes in basal gene expression and histone modification revealed that chronic IL-1 exposure alters transcriptional reprogramming and chromatin remodeling. Together, these findings demonstrate that chronic IL-1 signaling drives selective inflammatory response in hormone receptor–positive MCF7 and T47D breast cancer cells. This work underscores the continued therapeutic relevance of hormone receptor–targeted strategies in chronically inflamed tumors and provides insight into how sustained inflammatory stress shapes tumor behavior and gene regulation predicted to promote tumor progression.
2026-07-22 | GSE335261 | GEO
Project description:Asthma is a chronic inflammatory airway disease characterized by airway inflammation and remodeling. The role of 15-oxo-5Z,8Z,11Z,13E-eicosatetraenoic acid (15-oxoETE), a 15-HETE metabolite catalyzed by 15-prostaglandin dehydrogenase (15-PGDH), has been relatively unexplored in asthma. In this study, we used RNA-seq to explore the effect of 15-KETE on the transcriptome of airway epithelial cells, aiming to identify its potential downstream targets and mechanisms of action.
2026-05-21 | GSE325003 | GEO