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Expression data for MALT1-responsive genes

ABSTRACT: In lymphocyte lineages, mucosa-associated lymphoid tissue 1 (MALT1) mediates the nuclear factor-κB activation signal that stimulates progression of malignant tumors. However, its expression is inactivated in oral carcinoma patients with worse prognosis. Unveiling genes under the control of MALT1 will provide valuable information for understanding of the mechanism of carcinoma progression. We profiled gene datasets altered in response to MALT1 in oral carcinoma cells by the microarray analysis. Totally, 2,933 genes with a fold change ≥ ±2.0 and P < 0.05 were identified.

ORGANISM(S): Homo sapiens

PROVIDER: GSE42335 | GEO | 2013/06/18

SECONDARY ACCESSION(S): PRJNA181102

REPOSITORIES: GEO

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Expression data for MALT1-responsive genes

Project description:In lymphocyte lineages, mucosa-associated lymphoid tissue 1 (MALT1) mediates the nuclear factor-M-NM-:B activation signal that stimulates progression of malignant tumors. However, its expression is inactivated in oral carcinoma patients with worse prognosis. Unveiling genes under the control of MALT1 will provide valuable information for understanding of the mechanism of carcinoma progression. We profiled gene datasets altered in response to MALT1 in oral carcinoma cells by the microarray analysis. Totally, 2,933 genes with a fold change M-bM-^IM-% M-BM-12.0 and P < 0.05 were identified. HSC2 oral carcinoma cells were used for RNA extraction and hybridization on Affimetrix microarrays. We sought to obtain homogenous populations of MALT1-resonsive genes in order to increase the resolution of expression profiles. To this end, we used HSC2 cells stably expressing MALT1 (n=3) and vector alone (n=3) for the analysis.

2013-06-18 | E-GEOD-42335 | biostudies-arrayexpress

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Project description:Purpose: study the role of MALT1 auto-proteolysis in T cell receptor mediated activation of NF-kB. Methods: Jurkat cells were generated that express wild type MALT1, the auto-cleavage deficient MALT1-R149A mutant, the catalytic inactive MALT1-C464A mutant or the R149A-C464A double mutant (RACA). Expression of endogenous MALT1 was inactivated using TALEN technology for the Jurkat cells expressing MALT1-R149A (JDM-RA) and MALT1-C464A (JDM-CA). Illumina HISeq 2000 deep sequencing was performed to determine the mRNA profiles for MALT1, JDM-RA, JDM-CA and RACA cells in unstimulated conditions or after treatment with 75ng/ml PMA and 150 ng/ml ionomycin for 3 or 18 hrs. Results: PMA ionomycin stimulation of the MALT1 auto-cleavage defective JDM-RA cells fails to activate NF-kB-dependent transcription like for the MALT1 catalytic inactive JDM-CA cells and the double RACA mutant cells. Conclusion: MALT1 autoproteolysis is essential for transcription of NF-kB target genes

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Project description:To understand potential downstream signaling molecules that are responsible for wild type-Malt1 induced resistance of tumor cell to CD8 T cell killing , we first use E0771 cells expressing either -Vector control, wild type-Malt1 (M-WT), or Malt1 PD mutant (M-PD) to coculture with activated CD8 T cell at a effctor: target ratio(E:T ration) of 3 for 12 hours. Then wash the cells with PBS, digest the cells by 0.25% trypsin solution, harvest the cells in 15 ml tubes by centrifugation (1000 rpm 5min) and seed cells into the original plate with DMEM+10%FBS+1%P/S medium. 6 hours after sseding, wash cells with PBS, lyse cells with TRIZOL for RNA extraction, perform reverse transcription and cDNA library for RNA-Seq analysis.

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