Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA290335 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:STAiR18, an mRNA-like STAT3-induced long noncoding RNA shows ubiquitous expression. RNAi-mediated knockdown of STAiR18 led to a dramatic decrease in INA-6 cell vitality. Furthermore, STAiR18 knockdown reduced the STAT3 RNA and protein levels in these cells, suggesting a positive feedback loop between STAT3 and its target ncRNA STAiR18. Microarray analyses of INA-6 cells after STAiR18 or STAT3 knockdown revealed overlapping changes of transcription patterns indicating a close functional interplay between the two molecules. Taken together, STAiR18 represents a novel noncoding RNA that is likely to play an important role for the oncogenic function of the STAT3 pathway. STAT3- and STAiR18-dependent gene expression in human multiple myeloma cell line INA-6 was measured 40 hours after transfection with either a negative control siRNA, an siRNA to STAT3 or an siRNA to STAiR18. Four independent experiments were performed for each siRNA approach, yielding 12 approaches in total.
2016-07-17 | E-GEOD-71092 | biostudies-arrayexpress
Project description:STAiR18, an mRNA-like STAT3-induced long noncoding RNA shows ubiquitous expression. RNAi-mediated knockdown of STAiR18 led to a dramatic decrease in INA-6 cell vitality. Furthermore, STAiR18 knockdown reduced the STAT3 RNA and protein levels in these cells, suggesting a positive feedback loop between STAT3 and its target ncRNA STAiR18. Microarray analyses of INA-6 cells after STAiR18 or STAT3 knockdown revealed overlapping changes of transcription patterns indicating a close functional interplay between the two molecules. Taken together, STAiR18 represents a novel noncoding RNA that is likely to play an important role for the oncogenic function of the STAT3 pathway.
2016-07-17 | GSE71092 | GEO
Project description:Interleukin 6 (IL-6) activates the transcription factor signal transducer and activator of transcription 3 (STAT3). We previously identified several STAT3-induced long noncoding RNAs (STAiRs) in INA-6 multiple myeloma cells (Hackermüller et al. 2014). Here, we analyze five STAiRs by CAPTURE- and ChIRP-RNA-sequencing, a pulldown of a target RNA by transcript tiling oligonucleotides. The CAPTURE technique allows the identification of different STAiR splice variants and shall give rise to the transcript architecture. ChIRP, a method first published by Chu et al 2011, is the original method on which the CAPTURE approach is based on and enables the identification of RNAs interacting with our STAiRs.
2017-08-01 | GSE95131 | GEO
Project description:1. Evaluate the diagnostic value of long noncoding RNA (CCAT1) expression by RT-PCR in peripheral blood in colorectal cancer patients versus normal healthy control personal.
2. Evaluate the clinical utility of detecting long noncoding RNA (CCAT1) expression in diagnosis of colorectal cancer patients & its relation to tumor staging.
3. Evaluate the clinical utility of detecting long noncoding RNA (CCAT1) expression in precancerous colorectal diseases.
4. Compare long noncoding RNA (CCAT1) expression with traditional marker; carcinoembryonic antigen (CEA) and Carbohydrate antigen 19-9 (CA19-9) in diagnosis of colorectal cancer.
| 2330122 | ecrin-mdr-crc
Project description:Identification of splice variants and RNA binding partners of STAT3-induced long noncoding RNAs (STAiRs) in multiple myeloma
| PRJNA376176 | ENA
Project description:Analysis of gene expression alterations and RNA splicing events after Ancistrocladinium A treatment of INA-6 multiple myeloma cell line Ancistrocladinium A inan N,C-coupled naphthylisoquinoline alkaloid was analyzed for its ability to act as efficient anti-myeloma agent. The mode of action was unknown. We analyzed the effect of Ancistrocladinium A on the multiple myeloma cell line INA-6 on RNA level and identivied differentially regulated genes on the one hand and splicing events on the other hand gaining a first insight into the mode of action of Ancistrocladinium A.
2023-08-30 | GSE236602 | GEO
Project description:Multiple myeloma involves early dissemination of malignant plasma cells across the bone marrow; however, the initial steps of dissemination remain unclear. Human bone marrow-derived mesenchymal stromal cells (hMSCs) stimulate myeloma cell expansion (e.g., IL-6) and simultaneously retain myeloma cells via chemokines (e.g., CXCL12) and adhesion factors. Hence, we hypothesized that the imbalance between cell division and retention drives dissemination. We present an in vitro model using primary hMSCs co-cultured with INA-6 myeloma cells. Time-lapse microscopy revealed proliferation and attachment/detachment dynamics. Separation techniques (V-well adhesion assay and well plate sandwich centrifugation) were established to isolate MSC-interacting myeloma subpopulations that were characterized by RNAseq, cell viability and apoptosis. Results were correlated with gene expression data (n=837) and survival of myeloma patients (n=536). On dispersed hMSCs, INA-6 saturate hMSC-surface before proliferating into large homotypic aggregates, from which single cells detached completely. On confluent hMSCs, aggregates were replaced by strong heterotypic hMSC-INA-6 interactions, which modulated apoptosis time-dependently. Only INA-6 daughter cells (nMA-INA6) detached from hMSCs by cell division but sustained adherence to hMSC-adhering mother cells (MA-INA6). Isolated nMA-INA6 indicated hMSC-autonomy through superior viability after IL6 withdrawal and upregulation of proliferation-related genes. MA-INA6 upregulated adhesion and retention factors (CXCL12), that, intriguingly, were highly expressed in myeloma samples from patients with longer overall and progression-free survival, but their expression decreased in relapsed myeloma samples. Altogether, in vitro dissemination of INA-6 is driven by detaching daughter cells after a cycle of hMSC-(re)attachment and proliferation, involving adhesion factors that represent a bone marrow-retentive phenotype with potential clinical relevance.
2024-04-11 | GSE261423 | GEO
Project description:Abnormal NF-kB2 activation has been reported in several types of human leukemia and lymphomas although the exact mechanisms and affected pathways are not clear. We have investigated these questions through the use of a unique transgenic mouse model with lymphocyte-targeted expression of p80HT, a lymphoma associated NF-kB2 mutant. Microarray analysis, verified at the RNA and protein level identified new downstream targets and confirmed established regulatory networks. 201 genes were significantly changed, with 126 being upregulated and 75 downregulated. Pathway analysis uncovered both known and unknown interactions between factors important in the development of human B cell lymphomas and multiple myeloma, including cyclins D1 and D2, TRAF1, CD27, BIRC5/survivin, IL-15 and IL-10. Critical roles for STAT3 and TNF receptors are highlighted. Six target genes of STAT3 were identified: cyclins D1and D2, IL-10, survivin, IL-21 and Blimp1. Interfering with STAT3 signaling induced apoptosis in multiple myeloma cell lines. Novel pathways for NF-kB2 are proposed that involve IL-10 and other genes in the differentiation of plasma cells, evasion of apoptosis and proliferation. These pathways were verified with publically available human microarrays. Several treatment strategies based on these findings are discussed.
2012-12-31 | GSE30080 | GEO
Project description:Abnormal NF-kB2 activation has been reported in several types of human leukemia and lymphomas although the exact mechanisms and affected pathways are not clear. We have investigated these questions through the use of a unique transgenic mouse model with lymphocyte-targeted expression of p80HT, a lymphoma associated NF-kB2 mutant. Microarray analysis, verified at the RNA and protein level identified new downstream targets and confirmed established regulatory networks. 201 genes were significantly changed, with 126 being upregulated and 75 downregulated. Pathway analysis uncovered both known and unknown interactions between factors important in the development of human B cell lymphomas and multiple myeloma, including cyclins D1 and D2, TRAF1, CD27, BIRC5/survivin, IL-15 and IL-10. Critical roles for STAT3 and TNF receptors are highlighted. Six target genes of STAT3 were identified: cyclins D1and D2, IL-10, survivin, IL-21 and Blimp1. Interfering with STAT3 signaling induced apoptosis in multiple myeloma cell lines. Novel pathways for NF-kB2 are proposed that involve IL-10 and other genes in the differentiation of plasma cells, evasion of apoptosis and proliferation. These pathways were verified with publically available human microarrays. Several treatment strategies based on these findings are discussed. RNA was isolated from the B cells of p80HT transgenic mice on the C57BL/6J x SJL/J background , which produced serum monoclonal immunoglobulin (M-protein) (n=3), and the B cells from wild type (WT) littermates (n=3) using Trizol reagent according to the manufacturerM-bM-^@M-^Ys instructions (Invitrogen, Carlsbad, CA). RNA was further prepared with the Ambion WT Expression kit (Life Techologies Corp., Carlsbad, CA) then run on the Mouse Gene 1.0ST microarray chip (Affymetrix, Santa Clara, CA).
2012-12-31 | E-GEOD-30080 | biostudies-arrayexpress