RNA-seq analysis of human multiple myeloma cell line RPMI 8226 after HDAC1 knockdown
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PROVIDER: PRJNA795688 | ENA |
REPOSITORIES: ENA
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Project description:Histone deacetylases (HDACs) have emerged as therapeutic targets in multiple myeloma (MM); however, the underlying roles of each class- or isoform-HDAC have not fully clarified. The present study delineates the effect of HDAC1 suppression or inhibition in MM cells. The RNA-seq analysis here revealed that HDAC1 suppression downregulated IRF4 and PIM2, which both play a crucial role in MM cell survival and proliferation. Mechanistically, HDAC1 inhibition dampens IRF4 transcription through histone hyperacetylation and hindrance of RNA polymerase II recruitment at IRF4 locus. PIM2 is transcriptionally under direct regulation by IRF4, thereby reducing PIM2 expression after HDAC1 inhibition. PIM2 is upregulated by the stimuli from bone marrow microenvironment including IL-6 independent of IRF4 regulation in MM cells. Although these stimuli reduce the cytotoxic effect of HDAC1 inhibition in MM cells, direct blockade of PIM2 overcomes the weak point of HDAC1 inhibition. The effect of the combination of class I HDAC inhibitors with PIM inhibitors is further confirmed in vivo mouse xenograft models. Our findings provoke clinical applications of class I HDAC inhibitors in combination with PIM inhibitors against MM.
2022-09-21 | GSE193298 | GEO
Project description:Multiple Myeloma (MM) is an hematological malignancy. MM cells are resistant to X-ray irradiations. We irradiated RPMI 8226 cancer cells with C-ions, which are more energetic than X-ray irradiations. We found that MM cells, RPMI 8226, are also resistant to C-ion irradiations. We used microarrays to investigate the mechanisms of MM cell resistance to C-ion irradiations.
2016-01-05 | GSE76471 | GEO
Project description:Multiple Myeloma (MM) is an hematological malignancy. MM cells are resistant to X-ray irradiations. We irradiated RPMI 8226 cancer cells with C-ions, which are more energetic than X-ray irradiations. We found that MM cells, RPMI 8226, are also resistant to C-ion irradiations. We used microarrays to investigate the mechanisms of MM cell resistance to C-ion irradiations. MM cells, RPMI 8226, were subjected to 0 or 6 Gy doses of C-ion irradiations. RNA were extratred from each batch of cells one day after irradiations and subjected to microarray analysis.
2016-01-05 | E-GEOD-76471 | biostudies-arrayexpress
Project description:Although new therapies have doubled the survival of multiple myeloma (MM) patients, this remains an incurable disease. It has been postulated that the so-called MM Cancer Stem Cells (MM-CSC) would be responsible for tumor initiation and relapse but their unequivocal identification remains unclear. Here, we investigated in a panel of MM cell lines the presence of CD20+ cells harboring a MM-CSC phenotype. Among the multiple cell lines investigated, only a small population of CD20dim+ cells (0.3%) in the RPMI-8226 cell line was found. CD20dim+ RPMI-8226 cells expressed the plasma cell markers CD38 and CD138 and were CD19-CD27-. Additionally, CD20dim+ RPMI-8226 cells did not exhibit stem-cell markers as shown by gene expression profiling and the aldehyde dehydrogenase (ALDH) assay. Moreover, we demonstrated that CD20dim+ RPMI-8226 cells are not essential for CB17-SCID mice engraftment and show lower self-renewal potential than the CD20- RPMI-8226 cells. These results do not support CD20+ expression for the identification of MM-CSC.
2012-02-27 | GSE33020 | GEO
Project description:Analysis of Multiple Myeloma Cell lines JJN-3 and RPMI gene expression following treated with GSK-J4 or Bortezomib
2016-08-21 | GSE60600 | GEO
Project description:The RPMI-8226 human multiple myeloma cell line was stably infected with either a validated shRNA against BMI1 or a control shRNA. RNA was prepared from these lines, +/- doxycycline induction and at various time points post-induction. Samples were hybridized on the Affymetrix U133plus2 human genome expression microarray. The RPMI-8226 human multiple myeloma cell line was stably infected with either a validated shRNA against BMI1 or a control shRNA. RNA was prepared from these lines, +/- doxycycline induction and at various time points post-induction. Samples were hybridized on the Affymetrix U133plus2 human genome expression microarray.
2010-06-09 | E-GEOD-21912 | biostudies-arrayexpress
Project description:The RPMI-8226 human multiple myeloma cell line was stably infected with either a validated shRNA against BMI1 or a control shRNA. RNA was prepared from these lines, +/- doxycycline induction and at various time points post-induction. Samples were hybridized on the Affymetrix U133plus2 human genome expression microarray.
2010-05-19 | GSE21912 | GEO
Project description:We used microarrays to examine changes in gene expression in multiple myeloma cell lines following treatment with arsenic trioxide and darinaparsin Experiment Overall Design: Four multiple myeloma cell lines (U266, MM.1s, KMS11, 8226/S) were treated with either arsenic trioxide (ATO) for 6, 24, or 48 hours or darinaparsin (DAR) for 6 or 24 hours; RNA was extracted from treated and control cells for microarray analysis
2009-02-01 | E-GEOD-14519 | biostudies-arrayexpress
Project description:Comparison of gene expression profiles between CD138+ and CD138- populations from human myeloma cell lines RPMI-8226 and NCI-H929. We used Affymetrix human gene 1.0ST array and analyzed with GeneSpring GX.
2013-07-17 | GSE31305 | GEO
Project description:Leflunomide, an anti-inflammatory agent, has been shown to be effective in multiple myeloma (MM) treatment; however, the mechanism of this phenomenon has not been fully elucidated. The aim of the study was to assess the role of mitochondria and dihydroorotate dehydrogenase (DHODH) inhibition in the cytotoxicity of leflunomide in relation to the MM cell line RPMI 8226. The cytotoxic effect of teriflunomide-an active metabolite of leflunomide-was determined using MTT assay, apoptosis detection, and cell cycle analysis. To evaluate DHODH-dependent toxicity, the cultures treated with teriflunomide were supplemented with uridine. Additionally, the level of cellular thiols as oxidative stress symptom was measured as well as mitochondrial membrane potential and protein tyrosine kinases (PTK) activity. The localization of the compound in cell compartments was examined using HPLC method. Teriflunomide cytotoxicity was not abolished in uridine presence. Observed apoptosis occurred in a mitochondria-independent manner, there was also no decrease in cellular thiols level. Teriflunomide arrested cell cycle in the G2/M phase which is not typical for DHODH deficiency. PTK activity was decreased only at the highest drug concentration. Interestingly, teriflunomide was not detected in the mitochondria. The aforementioned results indicate DHODH- and mitochondria-independent mechanism of leflunomide toxicity against RPMI 8226 cell line.
| S-EPMC8469018 | biostudies-literature