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A small molecule screen identified N-Acetyl-L-cysteine for promoting ex vivo growth of single circulating tumor cell

ABSTRACT: A small molecule screen identified N-Acetyl-L-cysteine for promoting ex vivo growth of single circulating tumor cell

PROVIDER: PRJNA554073 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9670560.fastq.gz	Fastqsanger.gz
	SRR9670570.fastq.gz	Fastqsanger.gz
	SRR9670580.fastq.gz	Fastqsanger.gz
	SRR9670561.fastq.gz	Fastqsanger.gz
	SRR9670571.fastq.gz	Fastqsanger.gz

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A small molecule screen identified N-Acetyl-L-cysteine for promoting ex vivo growth of single circulating tumor cell

Project description:CTCs contain a small subset of metastatic precursors that can form metastases in secondary organs, and provide a resource to identify mechanisms underlying metastasis-initiating properties. Despite technological advancements that allow for highly sensitive approaches of detection and isolation, CTCs are very rare and often present as single cells, posing an extreme challenge for ex vivo expansion after isolation. Here, using previously established patient-derived CTC lines, we performed a small molecule drug screening to identify compounds that can improve ex vivo culture efficiency for single CTCs. We found that N-acetylcysteine (NAC) and other antioxidants can promote ex vivo expansion of single CTCs, facilitating subsequent functional analyses.

2022-07-07 | GSE134138 | GEO

Transcription profiling of human N-Acetyl L-cysteine induced differentiation of NHEK cells in vitro

Project description:Gene expression analysis of N-Acetyl L-cysteine induced differentiation of NHEK cells in vitro.

2005-11-30 | E-MEXP-500 | biostudies-arrayexpress

Transcriptional responses to maternal trichloroethylene and/or N-acetyl cysteine exposure in Wistar rat placental tissue

Project description:Trichloroethylene (TCE) is a persistent and pervasive environmental contaminant. N-acetyl cysteine (NAC) is an antioxidant that may reduce TCE effects. Pregnant Wistar rats were exposed to 480 mg TCE mg/kg/day, 200 mg/kg/day NAC or co-exposure with both chemicals via ingestion (mini vanilla wafer) on gestation days 6-16 (tissue collection day). TCE- and/or NAC-induced changes to gene expression were evaluated in male and female rat placentae.

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N-Acetyl-L-cysteine facilitates tendon repair and promotes the tenogenic differentiation of tendon stem/progenitor cells by enhancing the integrin α5/β1/PI3K/AKT signaling

Project description:N-acetyl-L-cysteine (NAC) is a potent antioxidant. However, how NAC affects the biological functions of tendon stem/progenitor cells (TSPCs) and tendon repair has not been clarified.The effect of NAC on gene transcription in TSPCs was analyzed by transcriptomes and bioinformatics.

2022-11-18 | GSE218038 | GEO

Acetyl-CoA is a Key Molecule for Nephron Progenitor Cell Pool Maintenance

Project description:Acetyl-CoA is a Key Molecule for Nephron Progenitor Cell Pool Maintenance

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Ex Vivo Lung Perfusion as a Human Platform for Preclinical Small Molecule Testing

Project description:We report mRNA expression from human lung homogenate samples taken during Ex Vivo Lung Perfusion during an acute challenge with LPS and an intervention with the small molecule BC1215

2018-08-16 | GSE118566 | GEO

Transcriptional responses to maternal trichloroethylene and/or N-acetyl cysteine exposure in Wistar rat placental tissue

Project description:Transcriptional responses to maternal trichloroethylene and/or N-acetyl cysteine exposure in Wistar rat placental tissue

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Feed-forward Cysteine Regulation Maintains Melanoma Differentiation State and Limits Metastatic Spread

Project description:The inherent ability of melanoma cells to alter the differentiation-associated transcriptional repertoire to evade treatment and facilitate metastatic spread is well accepted and has been termed phenotypic switching. However, how these facets of cellular behavior are controlled remains largely elusive. Here we show that cysteine availability, whether from lysosomes (CTNS-dependent) or exogenously derived (SLC7A11-dependent or as N-acetylcysteine), controls melanoma differentiation-associated pathways by acting on the melanocyte master regulator MITF. Functional data indicate that low cysteine availability reduces MITF levels and impairs lysosome functions, which affects tumor ferroptosis sensitivity but improves metastatic spread in vivo. Mechanistically, cysteine-restrictive conditions reduce acetyl-CoA levels to decrease p300-mediated H3K27 acetylation at the melanocyte-restricted MITF promoter, thus forming a cysteine feed-forward regulation that controls MITF levels and downstream lysosome functions. These findings collectively suggest that cysteine homeostasis governs melanoma differentiation by maintaining MITF levels and lysosome functions, which protect against ferroptosis and limit metastatic spread.

2024-08-16 | GSE269922 | GEO

N-Acetyl-L-Cysteine Reduces Cervical Carcinogenesis by Promoting Apoptosis.

Project description:Background and objectiveCervical cancer is the fourth leading cause of cancer death in women, and is one of the most common malignant tumors of the reproductive system. However, more effective treatment for cervical cancer is needed. In this study, we aim to investigate whether N-acetyl-L-cysteine (NAC) could inhibit the proliferation of human papillomavirus (HPV)-positive cells, and reduce cervical carcinogenesis.MethodsThe cervical cancer cell lines SiHa, HeLa, HPV-negative cell line C33A, and the immortalized human cervical keratinocyte cells S12 were used. The protein expression was determined using Western blot assay. mRNA expression was determined using quantitative reverse transcription polymerase chain reaction (qRT-PCR). Cell proliferation was determined by Cell Counting Kit-8 assay. Cell apoptosis was evaluated using Annexin V-FITC apoptosis kits. The numbers of colonies were measured using colony-forming assay. Xenograft tumor necrosis and HPV16 E7 expression were determined using hematoxylin and eosin (H&E) staining and immunohistochemistry.ResultsOur results showed that NAC treatment at the concentration of 1.5 mM significantly promoted cell apoptosis and reduced cell growth by inhibiting HPV16 E7 expression. NAC inhibited HPV16-oncoprotein-induced hypoxia-inducible factor (HIF)-1α protein expression and Akt activation in vitro. Additionally, NAC suppressed tumor growth, as evidenced by the smaller tumor size in the xenograft mouse model and decreased HPV16 E7 expression in tumor tissues.ConclusionOur findings demonstrate that NAC exhibits the potential to promote HPV-positive cell apoptosis, and suppress the proliferation of HPV-positive cells by inhibiting cell inhibitor of apoptosis protein 2 and HIF-1α.

| S-EPMC10293158 | biostudies-literature

Ex Vivo Lung Perfusion as a Human Platform for Preclinical Small Molecule Testing

Project description:Ex Vivo Lung Perfusion as a Human Platform for Preclinical Small Molecule Testing

| PRJNA486099 | ENA