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RNA sequencing of A549 lung cancer cells treated with a copper(I) bisphosphine complex (Complex 1)

ABSTRACT: Copper-based complexes are emerging as promising anticancer agents, yet their mechanisms of action remain incompletely understood. In this study, we evaluated a series of novel bisphosphine copper(I) thiocarbamide complexes and identified Complex 1, a bis(triphenylphosphine) copper(I) iodide complex bearing a thiocarbamide ligand, as exhibiting selective cytotoxicity toward lung cancer cells with reduced toxicity in normal fibroblasts. To elucidate its mechanism of action, whole transcriptome profiling was conducted on A549 cells following treatment with Complex 1. Cells were treated with 5 µM Complex 1 or vehicle control (DMSO) for 72 hours prior to RNA extraction. Differential gene expression analysis revealed modulation of pathways associated with p53 signalling, NF-κB signalling, and cell cycle regulation. These findings were supported by functional assays showing G2/M cell cycle arrest, indicating disruption of cell cycle progression as a primary mode of action, with apoptosis contributing to a lesser extent. Overall, this study demonstrates that novel bisphosphine copper(I) thiocarbamide complexes can exert selective anticancer activity and provides mechanistic insight into their effects on cancer-associated signalling networks, supporting their further development as therapeutic candidates.

ORGANISM(S): Homo sapiens

PROVIDER: GSE329396 | GEO | 2026/05/14

REPOSITORIES: GEO

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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.

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RNA sequencing of A549 lung cancer cells treated with a copper(I) bisphosphine complex (Complex 1)

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