Expression data of cHL cell lines after KLF4 activation
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE21296 | GEO | 2010/10/22
SECONDARY ACCESSION(S): PRJNA126243
REPOSITORIES: GEO
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Project description:FOXO1 is highly expressed in normal B cells and in most types of non-Hodgkinl lymphoma. In Hodgkin and Reed-Sternberg cells of classical Hodgkin lymphoma(cHL) expression of FOXO1 is low or absent. We overexpressed constitutively active mutant of FOXO1 fused in frame with estrogen receptor ligand-binding domain (FOXO1(3A)ER), which can be activated by 4-Hydroxytamoxifen (4-OHT), in cHL cell lines KM-H2 and L428. Activation of the FOXO1 with 4-OHT resulted in inhibition of proliferation and apoptosis. Using gene-expression array we found that FOXO1 activates transcription of known and potential tumor suppressor genes: CDKN1B, PMAIP1, BCL2L11, TNFSF10, FBXO32, CBLB). Of note, FOXO1 repressed transcription of several cytokines and cytokine receptors, which are known tobe involved in pathogenesis of cHL (e.g. CCL5, CXCR5, TNFRSF8). Taken togather our data indicate important role of FOXO1 repression in pathogenesis of cHL. KM-H2 and L428 cells expressing constitutively active mutant of human FOXO1 fused in frame with estrogen receptor ligand-binding domain were incubated with 200 µM 4-OHT or vehicle (ethanol). After 24 h, total RNA was isolated with RNeasy mini kit (QIAGEN). Microarray analyses were performed using 200 ng of total RNA as starting material and 5.5 µg ssDNA per hybridization (GeneChip Fluidics Station 450; Affymetrix, Santa Clara, CA). The total RNAs were amplified and labeled following the Whole Transcript (WT) Sense Target Labeling Assay (http://www.affymetrix.com). Labeled ssDNA was hybridized to Human Gene 1.0 ST Affymetrix GeneChip arrays (Affymetrix, Santa Clara, CA). The chips were scanned with a Affymetrix GeneChip Scanner 3000 and subsequent images analyzed using Affymetrix® Expression Console Software (Affymetrix). Probe level data were obtained using the robust multichip average (RMA) normalization algorithm.
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Project description:In this study, we examined if KLF4 and c-MYC (KM)-transduced murine cardiac mesenchymal progenitors (CMPs) played a role in the differentiation into adipocytes in the absence of adipogenic stimulation cocktails. These progenitors exhibited increased expression of adipogenic-related genes, such as C/EBPα, PPARγ, and Fabp4, activation of the PPAR signaling pathway, and formation of cytoplasmic lipid droplets within 10 days. Moreover, these KM genes sharply increased following a reperfusion insult, resulting in increased ectopic fat formation. Thus, understanding CMP adipogenesis will clarify the pathophysiology of ischemic reperfusion injury and myocardial infarction and may pave the way for better treatment strategies.
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