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Overexpression of RNA polymerase I specific SL1 component TAF1C induces cancer-specific gene expression in BEAS-2B cells

ABSTRACT: Purpose: Hyperactive RNA Polymerase I (Pol I) transcription and the upregulation of proteins essential for the initiation of Pol I transcription are the common features of a wide range of cancers . However, the role of Pol I transcription in the etiology of cancer remains unclear. Here, we activated Pol I transcription by overexpressing SL1 subunit TAF1C, and performed whole transcriptome analysis by RNA-Seq. Methods: Non-cancerous lung epithelial BEAS-2B cellswere transfected with empty vector (eV) and TAF1C expression vector (TAF1C) to generate stable cell lines. Total RNA was isolated from biological triplicates of eV and TAF1C BEAS-2B stable cells and used for RNA sequencing on Illumina platform. Results: The whole transcriptomics data revealed the upregulation of cancer related genes in BEAS-2B cells stably expressing TAF1C gene. Integration of whole transcriptome data revealed interactive regulatory networks between protein-coding RNAs, lncRNAs and miRNAs associated with various hallmarks of cancer. Conclusions: For the first time, we provide evidence for the global gene expression changes in response to activated Pol I transcription in the context of cancer. The regulatory networks identified in the study can further be validated as potential drug targets for cancer therapeutics

ORGANISM(S): Homo sapiens

PROVIDER: GSE198601 | GEO | 2025/03/11

REPOSITORIES: GEO

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Project description:As environmental pollutants and possible carcinogens, carbon nanotubes (CNTs) have recently been found to promote tumorigenesis and tumor metastasis after long-term pulmonary exposure. However, whether CNT-induced carcinogenesis can be inherited and last for generations remains unknown. Here, we establish a post-chronic single-walled carbon nanotubes (SWCNTs) exposed human bronchial epithelium BEAS-2B cell model to investigate SWCNTs-induced carcinogenesis. At a tolerated sublethal dose level, post-chronic SWCNTs exposure significantly increases the migration and colony formation abilities of BEAS-2B cells, leading to cell malignant transformation. Notably, the malignant transformation of BEAS-2B cells is irreversible within 60 days recovery period after SWCNTs exposure, and the malignant transformation activities of cells gradually increase during the recovery period. Mechanism analyses show that post-chronic exposure to SWCNTs causes substantial DNA methylation and transcriptome dysregulation of BEAS-2B cells. Subsequent enrichment and clinical database analyses reveal that differentially expressed/methylated genes of BEAS-2B cells are enriched in cancer-related biological pathways, and several of these genes are validated in lung cancer patients. As environmental pollutants and possible carcinogens, carbon nanotubes (CNTs) have recently been found to promote tumorigenesis and tumor metastasis after long-term pulmonary exposure. However, whether CNT-induced carcinogenesis can be inherited and last for generations remains unknown. Here, we establish a post-chronic single-walled carbon nanotubes (SWCNTs) exposed human bronchial epithelium BEAS-2B cell model to investigate SWCNTs-induced carcinogenesis. At a tolerated sublethal dose level, post-chronic SWCNTs exposure significantly increases the migration and colony formation abilities of BEAS-2B cells, leading to cell malignant transformation. Notably, the malignant transformation of BEAS-2B cells is irreversible within 60 days recovery period after SWCNTs exposure, and the malignant transformation activities of cells gradually increase during the recovery period. Mechanism analyses show that post-chronic exposure to SWCNTs causes substantial DNA methylation and transcriptome dysregulation of BEAS-2B cells. Subsequent enrichment and clinical database analyses reveal that differentially expressed/methylated genes of BEAS-2B cells are enriched in cancer-related biological pathways, and several of these genes are validated in lung cancer patients.

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Overexpression of RNA polymerase I specific SL1 component TAF1C induces cancer-specific gene expression in BEAS-2B cells

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