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Transcriptome analysis for the effect of Trichostatin A on intrahepatic cholangiocarcinoma cells

ABSTRACT: Trichostatin A (TSA) is a commonly used antifungal drug characterized by inhibiting the activity of histone deacetylases (HDACs). As an antineoplastic agent, the pharmacological actions of TSA includes: 1. Inhibiting the proliferation of tumor cells directly; 2. Promoting the antitumor effect of immune cells; 3. Enhancing the efficacy of other antitumor drugs. The efficacy of TSA in the treatment of intrahepatic cholangiocarcinoma (ICCA) is still unknown and needs further verification. Therefore, in this study, ICCA cell line HUCCT1 was treated by TSA. The total RNA samples were used for transcriptome analysis to find the potential target of HDACs.

ORGANISM(S): Homo sapiens

PROVIDER: GSE252094 | GEO | 2025/01/20

REPOSITORIES: GEO

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Project description:The use of gene expression signatures to classify compounds, identify efficacy or toxicity, and differentiate close analogs relies on the sensitivity of the method to identify modulated genes. We used a novel ligation-based targeted whole transcriptome expression profiling assay, TempO-Seq®, to determine whether previously unreported compound-responsive genes could be identified and incorporated into a broad but specific compound signature. TempO-Seq exhibits 99.6% specificity, single cell sensitivity, and excellent correlation with fold differences measured by RNA-Seq (R2 = 0.9) for 20,629 targets. Unlike many expression assays, TempO-Seq does not require RNA purification, cDNA synthesis, or capture of targeted RNA, and lacks a 3′ end bias. To investigate the sensitivity of the TempO-Seq assay to identify significantly modulated compound-responsive genes, we derived whole transcriptome profiles from MCF-7 cells treated with the histone deacetylase inhibitor Trichostatin A (TSA) and identified more than 9,000 differentially expressed genes. The TSA profile for MCF-7 cells overlapped those for HL-60 and PC-3 cells in the Connectivity Map (cMAP) database, suggesting a common TSA-specific expression profile independent of baseline gene expression. A 43-gene cell-independent TSA signature was extracted from cMAP and confirmed in TempO-Seq MCF-7 data. Additional genes that were not previously reported to be TSA responsive in the cMAP database were also identified. TSA treatment of 5 cell types revealed 1,136 differentially expressed genes in common, including 785 genes not previously reported to be TSA responsive. We conclude that TSA induces a specific expression signature that is consistent across widely different cell types, that this signature contains genes not previously associated with TSA responses, and that TempO-Seq provides the sensitive differential expression detection needed to define such compound-specific, cell-independent, changes in expression.

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Transcriptome analysis for the effect of Trichostatin A on intrahepatic cholangiocarcinoma cells

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