Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA120665 | ENA |
REPOSITORIES: ENA
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Project description:During cancer progression, carcinoma cells encounter a variety of cytotoxic stresses such as hypoxia, nutrient deprivation, and low pH as a result of inadequate vascularization. To maintain survival and growth in the face of these physiologic stressors, a set of adaptive response pathways are induced. One adaptive pathway well studied in other contexts is the unfolded protein response (UPR), of which XBP1 is an important component. We used microarrays to detect transcriptome profile changes after XBP1 knockdown in breast cancer cell lines, and identify genes and pathways regulated by XBP1, which could help elucidate how XBP1 mediates the adaptive response of breast cancer to cytotoxic stresses. We extracted RNA and hybridized it to Affymetrix microarrays in two breast cancer cell lines (T47D and MDA-MB-231) under treated (hypoxia and glucose deprivation) or untreated conditions with XBP1 knockdown or not.
2013-09-26 | E-GEOD-49953 | biostudies-arrayexpress
Project description:During cancer progression, carcinoma cells encounter a variety of cytotoxic stresses such as hypoxia, nutrient deprivation, and low pH as a result of inadequate vascularization. To maintain survival and growth in the face of these physiologic stressors, a set of adaptive response pathways are induced. One adaptive pathway well studied in other contexts is the unfolded protein response (UPR), of which XBP1 is an important component. We used microarrays to detect transcriptome profile changes after XBP1 knockdown in breast cancer cell lines, and identify genes and pathways regulated by XBP1, which could help elucidate how XBP1 mediates the adaptive response of breast cancer to cytotoxic stresses.
2013-09-26 | GSE49953 | GEO
Project description:Self-sufficiency (autonomy) in growth signaling, the earliest recognized hallmark of cancer, is fuelled by the tumor cell’s ability to ‘secrete-and-sense’ growth factors; this translates into cell survival and proliferation that is self-sustained by auto-/paracrine secretion. Using breast cancer cells that are either endowed or inept in growth signaling autonomy, here we reveal how tumor cell autonomy impacts cancer progression. Autonomy is associated with enhanced molecular programs for stemness, immune evasiveness, and epithelial-mesenchymal plasticity (EMP) across the entire mesenchymal spectrum. Autonomy is both necessary and sufficient for anchorage-independent growth factor-restricted growth, resistance to anti-cancer drugs and metastatic progression. Transcriptomic and proteomic studies show that autonomy is associated with self-sustained EGFR/ERBB signaling, a required signal for re-epithelialization. A gene expression signature was derived (a.k.a., autonomy signature) which revealed that autonomy is induced in circulating tumor cells (CTCs), the precursor tumor cells that re-epithelialize to initiate metastases. Autonomy in CTCs tracks therapeutic response and prognosticates outcome. Autonomy is present during reversible (but not stable) EMT and requires EGFR/ERBB signaling. These data support a role for growth signaling autonomy in the blood-borne dissemination of human breast cancer.
2023-02-06 | PXD037253 | Pride
Project description:Natural Killer (NK) cells are innate cytotoxic lymphocytes with adaptive immune features, including antigen-specificity, clonal expansion, and memory. As such, NK cells share many transcriptional and epigenetic programs with their adaptive CD8+ T cell siblings. Various signals ranging from antigen, co-stimulation, and proinflammatory cytokines are required for optimal NK cell responses in mice and humans during virus infection; however, the integration of these signals remains unclear. In this study, we identified the transcription factor IRF4 as a signal integrator to coordinate the NK cell response during viral infection. Loss of IRF4 was detrimental to the expansion and differentiation of virus-specific NK cells. This defect was partially attributed to the inability of IRF4-deficient NK cells to uptake nutrients required for survival and memory generation. Altogether, these data suggest IRF4 is a signal integrator that acts as a secondary metabolic checkpoint to orchestrate the adaptive response of NK cells during viral infection.
2023-08-03 | GSE235064 | GEO
Project description:Natural Killer (NK) cells are innate cytotoxic lymphocytes with adaptive immune features, including antigen-specificity, clonal expansion, and memory. As such, NK cells share many transcriptional and epigenetic programs with their adaptive CD8+ T cell siblings. Various signals ranging from antigen, co-stimulation, and proinflammatory cytokines are required for optimal NK cell responses in mice and humans during virus infection; however, the integration of these signals remains unclear. In this study, we identified the transcription factor IRF4 as a signal integrator to coordinate the NK cell response during viral infection. Loss of IRF4 was detrimental to the expansion and differentiation of virus-specific NK cells. This defect was partially attributed to the inability of IRF4-deficient NK cells to uptake nutrients required for survival and memory generation. Altogether, these data suggest IRF4 is a signal integrator that acts as a secondary metabolic checkpoint to orchestrate the adaptive response of NK cells during viral infection.
2023-08-03 | GSE236555 | GEO
Project description:Using transgenic mouse models of breast cancer, we demonstrate that loss of ShcA signaling within mammary tumors results in extensive CD4+ T cell infiltration, activation and induction of a humoral immune response. Our studies reveal that ShcA signaling during early breast cancer progression is required to establish and maintain an immunosuppressive state that favors tumor growth. Consistent with these transgenic studies, high ShcA levels correlate with poor outcome and reduced CTL infiltration in primary human breast cancers. Conversely, elevated expression of a ShcA-regulated immune signature, generated from ShcA-null mammary tumors, is a predictor of good prognosis in HER2-positive and basal breast cancer patients. These observations define a novel role for ShcA in polarizing the immune response to facilitate tumorigenesis NIC SHC null Tumors vs. pooled MMPV-NIC reference, some replicate dye swaps
2010-10-12 | E-GEOD-18996 | biostudies-arrayexpress
Project description:Self-sufficiency (autonomy) in growth signaling, the earliest recognized hallmark of cancer, is fuelled by the tumor cell’s ability to ‘secrete-and-sense’ growth factors; this translates into cell survival and proliferation that is self-sustained by auto-/paracrine secretion. Using breast cancer cells that are either endowed or impaired in growth signaling autonomy, here we reveal how autonomy impacts cancer progression. Autonomy is associated with enhanced molecular programs for stemness, immune evasiveness, proliferation, and epithelial-mesenchymal plasticity (EMP). Autonomy is both necessary and sufficient for anchorage-independent growth factor-restricted proliferation and resistance to anti-cancer drugs and is required for metastatic progression. Transcriptomic and proteomic studies show that autonomy is associated with self-sustained EGFR/ErbB signaling. A gene expression signature is derived (a.k.a., autonomy signature) which revealed that autonomy is induced in circulating tumor cells (CTCs) and particularly CTC clusters, the latter of which carry higher metastatic potential. Autonomy in CTCs tracks therapeutic response and prognosticates outcome. Autonomy is preserved during reversible (but not stable) EMT. These data support a role for growth signaling autonomy in multiple processes essential for the blood-borne dissemination of human breast cancer.
2023-06-20 | GSE215822 | GEO
Project description:Mufudza2012 - Estrogen effect on the dynamics
of breast cancer
This deterministic model shows the
dynamics of breast cancer with immune response. The effects of
estrogen are incorporated to study its effects as a risk factor for
the disease.
This model is described in the article:
Assessing the effects of
estrogen on the dynamics of breast cancer.
Mufudza C, Sorofa W, Chiyaka
ET.
Comput Math Methods Med 2012; 2012:
473572
Abstract:
Worldwide, breast cancer has become the second most common
cancer in women. The disease has currently been named the most
deadly cancer in women but little is known on what causes the
disease. We present the effects of estrogen as a risk factor on
the dynamics of breast cancer. We develop a deterministic
mathematical model showing general dynamics of breast cancer
with immune response. This is a four-population model that
includes tumor cells, host cells, immune cells, and estrogen.
The effects of estrogen are then incorporated in the model. The
results show that the presence of extra estrogen increases the
risk of developing breast cancer.
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000642.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2017-07-26 | BIOMD0000000642 | BioModels
Project description:Using transgenic mouse models of breast cancer, we demonstrate that loss of ShcA signaling within mammary tumors results in extensive CD4+ T cell infiltration, activation and induction of a humoral immune response. Our studies reveal that ShcA signaling during early breast cancer progression is required to establish and maintain an immunosuppressive state that favors tumor growth. Consistent with these transgenic studies, high ShcA levels correlate with poor outcome and reduced CTL infiltration in primary human breast cancers. Conversely, elevated expression of a ShcA-regulated immune signature, generated from ShcA-null mammary tumors, is a predictor of good prognosis in HER2-positive and basal breast cancer patients. These observations define a novel role for ShcA in polarizing the immune response to facilitate tumorigenesis
2010-10-12 | GSE18996 | GEO
Project description:MicroRNAs expression profiling during breast cancer progression
| PRJNA169159 | ENA