Signalling via the colony stimulating factor 1 receptor (CSF1R) controls the survival, differentiation and proliferation of macrophages which are a source of the somatic growth factor insulin growth factor 1 (IGF1). Treatment of newborn mice with CSF1 has previously been shown to produce an increase in somatic growth rate and we hypothesised that treatment of neonatal low birth weight (LBW) rats with CSF1 would do the same. Growth rates were not affected, yet CSF1 treatment caused an unexpectedly large, but reversible increase in liver size and hepatic fat deposition in both normal and LBW rats. By transcriptional profiling, we have highlighted numerous CSF1-regulated genes known to be involved in lipid droplet formation in the liver and novel candidate genes for further investigation. In contrast to mice and weaner pigs, CSF1 treatment did not increase hepatocyte proliferation in neonatal rats, rather the data were consistent with increased macrophage proliferation instead. This suggests that Kupffer cells promote lipid accumulation in neonates and treatment to ablate CSF1R signalling may reverse lipid accumulation in the liver.
Macrophage colony-stimulating factor increases hepatic macrophage content, liver growth, and lipid accumulation in neonatal rats.
Specimen part, Treatment
View SamplesWe used RNA sequencing to study gene expression in lymph node derived DCs from anaphylactic mice sensitized intranasally with the major peach allergen Pru p 3, during the acute reaction phase, induced intraperitoneally. In total, 237 genes changed significantly, 181 showing at least two-fold changes. Almost three quarters of these increased during anaphylaxis Overall design: 5 Female Balb/c mice aged 4-5 weeks, were sensitized to peach using intranasally administered Pru p 3 in combination with LPS and challenged intraperitoneally as described previously . 5 Littermates, treated with intranasally administered PBS (instead of Pru p 3 and LPS), and later given an intraperitoneal challenge as per the anaphylactic mice, were used for comparison.
Transcriptional Profiling of Dendritic Cells in a Mouse Model of Food-Antigen-Induced Anaphylaxis Reveals the Upregulation of Multiple Immune-Related Pathways.
Sex, Cell line, Treatment, Subject
View SamplesERAS (Embryonic stem (ES) cell-expressed Ras) is a constitutively active member of the Ras family that is not expressed in adult tissues, and has been involved in breast cancer.
The Ras-related gene ERAS is involved in human and murine breast cancer.
Cell line
View SamplesGene expression from MCF7 breast cancer cells at different times of TNFa incubation:pcs2 and 14-3-3 transduced cells
Inhibition of specific NF-κB activity contributes to the tumor suppressor function of 14-3-3σ in breast cancer.
Time
View SamplesDUSP1 is involved in different cellular pathways including cancer cell proliferation, angiogenesis, invasion and resistance to chemotherapy. To understand more about the cellular responses regulated by DUSP1 in NSCLC cells, we interfered DUSP1 expression in the NSCLC cell line H460 and studied the changes in gene expression differentially regulated by this phosphatase.
DUSP1/MKP1 promotes angiogenesis, invasion and metastasis in non-small-cell lung cancer.
Specimen part, Cell line
View SamplesH69M cells derive from H69 small cell lung cancer cells subjected to prolonged treatment with HGF. Among the whole population of cells, a subset of more fibroblastic cells was isolated (H69M-mesenchymal). In this experiment we compared expression profiles of both cell lines
Targeting epithelial-to-mesenchymal transition with Met inhibitors reverts chemoresistance in small cell lung cancer.
Specimen part, Cell line
View SamplesNF-kB has been linked to doxorubicin-based chemotherapy resistance in breast cancer patients. NF-kB nuclear translocation and DNA binding in doxorubicin treated-breast cancer cells have been extensively examined, however its functional consequences in terms the spectrum of NF-kB -dependent genes expressed and, thus, the impact on tumour cell behaviour are unclear.
Deficiency in p53 is required for doxorubicin induced transcriptional activation of NF-кB target genes in human breast cancer.
Cell line, Treatment
View SamplesBackground: Interval breast cancers can occur through failure to detect an abnormality at the time of screening (missed interval cancer), or as a new event after a negative screen (true interval cancer). The development and progression of true interval tumors (TIBC) is known to be different than screen-detected tumors (SDBC). However, much work still needs to be done to understand the biological characteristics and clinical behaviour of these TIBC. Objectives: To characterize the gene expression profile in TIBC and SDBC aimed to identify biological markers that may be associated with the emergence of symptomatic breast cancer in the screening interval. Material and Methods: An unsupervised exploratory gene expression profile analysis was performed among 10 samples (discovery set, TIBC=5 and SDBC=5) using Affymetrix Human Gene 1.0 ST arrays and interpreted by Ingenuity Pathway Analysis. Differential expression of selected genes was confirmed in validation series of 91 patients (TIBC=12 and SDBC=79) by immunohistochemistry and 24 patients (TIBC=8 and SDBC=16) by RT-qPCR, expanding the analysis to other genes in same pathway (mTOR, 4E-BP1, eIF-4G and S6).
Gene expression profiling in true interval breast cancer reveals overactivation of the mTOR signaling pathway.
Specimen part
View SamplesThe 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)
FoxA and LIPG endothelial lipase control the uptake of extracellular lipids for breast cancer growth.
Cell line
View SamplesStress constantly challenges plant adaptation to the environment. Of all stress types, arsenic was a major threat during the early evolution of plants. The most prevalent chemical form of arsenic is arsenate, whose similarity to phosphate renders it easily incorporated into cells via the phosphate transporters. Here we found that arsenate stress provokes a notable transposon burst in plants, in coordination with arsenate/phosphate transporter repression, which immediately restricts arsenate uptake. This repression was accompanied by delocalization of the phosphate transporter from the plasma membrane. When arsenate was removed, the system rapidly restored transcriptional expression and membrane localization of the transporter. We identify WRKY6 as an arsenate-responsive transcription factor that mediates arsenate/phosphate transporter gene expression and restricts arsenate-induced transposon activation. Plants therefore have a dual WRKY-dependent signaling mechanism that modulates arsenate uptake and transposon expression, providing a coordinated strategy for arsenate tolerance and transposon gene silencing.
WRKY6 transcription factor restricts arsenate uptake and transposon activation in Arabidopsis.
Time
View Samples