Unknown,Transcriptomics,Genomics,Proteomics

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Transcriptional analysis (nCounter Human Immunology v2 Panel) of A549 cells with HMGB1 knockdown and infected with WT or attenuated mutant Dengue virus 2 strains

ABSTRACT: HMGB1 were silence in A549 cells using siRNA targeting.These A549 cells were then infected with WT Dengue virus 2 and its attenuated mutants (generated using infectious clone construction with site-directed mutagenesis) to better understand the gene expression changes induced by these different attenuated viruses and the role HMGB1 plays in this context.

ORGANISM(S): Homo sapiens

SUBMITTER: Justin Ooi

PROVIDER: E-MTAB-16204 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:The Sin3 histone deacetylase (HDAC) complex is a 1.2 MDa chromatin modifying complex that can repress transcription by binding to gene promoters and deacetylating histones. The Sin3/HDAC complex can affect cell cycle progression through multiple mechanisms and is among the targets of anticancer drugs, called HDAC inhibitors. We describe the identification of a new subunit of the Sin3 complex named family with sequence similarity 60 member A (FAM60A). We show that FAM60A/Sin3 complexes normally suppress the epithelial-to-mesenchymal transition (EMT) and cell migration. This occurs through transcriptional repression of genes that encode components of the TGF-beta signaling pathway. This work reveals that FAM60A and the Sin3 complex are upstream repressors of TGF-beta signaling, EMT and cell migration and extends the known biological roles of the Sin3 complex. This experiment investigates the role of FAM60A in gene expression by comparing A549 lung cancer cells treated with or without siRNA against FAM60A. The Sin3 histone deacetylase (HDAC) complex is a 1.2 MDa chromatin modifying complex that can repress transcription by binding to gene promoters and deacetylating histones. SDS3 is a core component of the Sin3 complex. The Sin3/HDAC complex can affect cell cycle progression through multiple mechanisms and is among the targets of anticancer drugs, called HDAC inhibitors. We describe the identification of a new subunit of the Sin3 complex named family with sequence similarity 60 member A (FAM60A). We show that FAM60A/Sin3 complexes normally suppress the epithelial-to-mesenchymal transition (EMT) and cell migration. This occurs through transcriptional repression of genes that encode components of the TGF-beta signaling pathway. This work reveals that FAM60A and the Sin3 complex are upstream repressors of TGF-beta signaling, EMT and cell migration and extends the known biological roles of the Sin3 complex. As a base line to better understand the relationship between FAM60A and the Sin3 complex, this experiment investigates the gene expression changes which occur in A549 lung cancer cells when the Sin3 complex is perturbed by knockdown of a core component via siRNA against SDS3. FAM60A siRNA knockdowns were compared to a non-targeting control in triplicate, for a total of 6 samples. SDS3 siRNA knockdowns were compared to a non-targeting control in triplicate, for a total of 6 samples.

Dataset Information

Transcriptional analysis (nCounter Human Immunology v2 Panel) of A549 cells with HMGB1 knockdown and infected with WT or attenuated mutant Dengue virus 2 strains

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