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Generic drug screen identifies paracetamol as 5-aza-2’-deoxycytidine sensitizer in head and neck squamous cell carcinoma cells

ABSTRACT: Generic drug screen identifies paracetamol as 5-aza-2’-deoxycytidine sensitizer in head and neck squamous cell carcinoma cells

PROVIDER: PRJNA432654 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6665450_1.fastq.gz	Fastqsanger.gz
	SRR6665450_2.fastq.gz	Fastqsanger.gz
	SRR6665451_1.fastq.gz	Fastqsanger.gz
	SRR6665451_2.fastq.gz	Fastqsanger.gz
	SRR6665452_1.fastq.gz	Fastqsanger.gz

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Generic drug screen identifies paracetamol as 5-aza-2’-deoxycytidine sensitizer in head and neck squamous cell carcinoma cells

Project description:Aberrant DNA methylation (5mC) is one of the key characteristics of many cancers including head and neck squamous cell carcinoma (HNSCC). The DNA demethylating agent 5-aza-2’-deoxycytidine (DAC) has anti-cancer therapeutic potential, but its clinical efficacy is currently hindered by dose-limiting side effects. Here we investigated the potential use of DAC in the treatment of HNSCC and show that its efficacy is primarily dependent on the ability of DAC to demethylate DNA. In order to establish whether HNSCC cells can be sensitized to DAC, a panel of 100 generic drugs were screened in combination with DAC. While the 100-drug panel did not sensitise DAC-resistant HNSCC cell lines to DAC treatment, the screen identified that paracetamol (acetaminophen), valproic acid and zinc acetate significantly enhanced DAC efficacy in the DAC-responsive cell lines. DAC and paracetamol were established to work in synergy, allowing DAC to be used at therapeutically relevant low doses (below 500nM). The mechanisms underlying the DAC-paracetamol synergy are multifactorial and encompass both effects of DAC on paracetamol action (alterations in the cyclooxygenase (COX) pathway and mimicry of paracetamol overdose) as well as decreased DNA methylation by paracetamol. Therefore, we propose DAC to be a potential therapeutic in a subset of HNSCC patients with its efficacy significantly increased by use of the common analgesic paracetamol. The DAC-paracetamol synergy should also be considered in cancers with an approved DAC treatment regime.

2018-11-02 | GSE110045 | GEO

MCF7 cells gene expression change by inducing CpG demethylation using 5-Aza-2'-deoxycytidine (Aza)

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SUMO pulldown proteomics Namalwa 5-Aza-2' deoxycytidine treatment

Project description:Combination therapies targeting malignancies aim to increase treatment efficacy and reduce toxicity. Hypomethylating drug 5-Aza-2’-deoxycytidine (5-Aza-2’) enhances transcription of tumor suppressor genes and induces replication errors via entrapment of DNMT1. Post-translational modification by SUMO plays major roles in the DNA damage response and is required for degradation of entrapped DNMT1. Here, we combine SUMOylation inhibitor TAK981 and DNA-hypomethylating agent 5-Aza-2’ to improve treatment of MYC driven hematopoietic malignancies, since MYC overexpressing tumors are sensitive to SUMOylation inhibition. We studied the classical MYC driven malignancy Burkitt lymphoma, as well as diffuse large B-cell lymphoma (DLBCL) with and without MYC translocation. SUMO inhibition prolonged the entrapment of DNMT1 to DNA, resulting in DNA damage. An increase in DNA damage was observed in cells co-treated with TAK981 and 5-Aza-2’. Both drugs synergized to reduce cell proliferation in vitro in a B cell lymphoma cell panel, including Burkitt lymphoma and DLBCL. In vivo experiments combining TAK981 (25 mg/kg) and 5-Aza-2’ (2.5 mg/kg) showed a significant reduction in outgrowth of Burkitt lymphoma in an orthotopic xenograft model. In contrast, single dosing of TAK981 was ineffective and single dosing of 5-Aza-2’ only led to a modest outgrowth reduction. TAK981 and 5-Aza-2’ synergize to reduce B cell Lymphoma outgrowth in vitro and in vivo. SUMOylation is a key-player in the repair of DNA damage, hence upon TAK981 treatment the repair of DNA damage induced by 5-Aza-2’ treatment is impaired. Our results demonstrate the potential of tailored combination of drugs, based on insight in molecular mechanisms, to improve the efficacy of cancer therapies.

2023-03-17 | PXD038620 | Pride

5-aza-2-deoxycytidine treatment of Swarm rat chondrosarcoma cells

2010-08-06 | GSE17598 | GEO

Expression microarray with 5-aza-2'-deoxycytidine-treated Caco-2 cells

Project description:5-aza-2'-deoxycytidine (DAC) treated and untreated Caco-2 cells were compared using an expression microarray.

2011-12-27 | GSE19660 | GEO

MCF7 cells gene expression change by inducing CpG demethylation using 5-Aza-2'-deoxycytidine (Aza)

Project description:Promoter methylation is able to induce downregulation of gene expression. 5-Aza-2'-deoxycytidine(Aza), methytransferase inhibitor, induce CpG demethylation. Here, 5-Aza-2'-deoxycytidine(Aza) is treated in a human breast cancer cell, MCF7, for detection of gene expression change. To analyze gene expression change by aza, control RNA isolated from MCF-7 was compared with RNA isolated from MCF-7 treated with 5uM and 10uM aza.

2011-08-17 | E-GEOD-31441 | biostudies-arrayexpress

SUMO pulldown, U2OS, proteomics, 4 hour 20 hour 5-Aza-2' deoxycytidine treatment

2023-03-17 | PXD038617 | Pride

Genome-wide DNA demethylation of TGW (neuroblastoma cell line) after treatment of mock and 5-aza-2'-deoxycytidine (5-aza-dC)

Project description:A neuroblasoma cell line, TGW, was treated with a DNA demethylating agents (5-aza-2'-deoxycytidine: 5-aza-dC). Genome-wide DNA methylation was analyzed using the Infinium Human MethylationEPIC BeadChip.

2021-07-23 | GSE180660 | GEO

Genome-wide DNA demethylation of NB-1 (neuroblastoma cell line) after treatment of mock and 5-aza-2'-deoxycytidine (5-aza-dC)

Project description:A neuroblasoma cell line, NB-1, was treated with a DNA demethylating agents (5-aza-2'-deoxycytidine: 5-aza-dC). Genome-wide DNA methylation was analyzed using the Infinium HumanMethylation450 BeadChip.

2021-07-29 | GSE180929 | GEO

5-aza-2-deoxycytidine treatment of Swarm rat chondrosarcoma cells

Project description:The puropose of this experiment was to identify gene expression changes that result from 5-aza-2-deoxycytidine induced DNA demethylation of Swarm rat chondrosarcoma cells. The gene expression profiles of untreated Swarm rat chondrosarcoma cells were compared to the gene expression profiles of Swarm rat chondrosarcoma cells that were treated for 5 passages with a low dose of 5-aza-2-deoxycytidine (0.1uM). Five chip study. For these experiments, microarray was carried out on untreated (control) Swarm rat chondrosarcoma cells (3 biological replicates), and microarray was also carried out on Swarm rat chondrosarcoma cells treated with 5-aza-2-deoxycytidine (2 biological replicates).

2010-08-06 | E-GEOD-17598 | biostudies-arrayexpress

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