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A novel MYC-ZNF706-SLC7A11 regulatory circuitry contributes to cancer progression and redox balance in human hepatocarcinoma (RNA-Seq)

ABSTRACT: A novel MYC-ZNF706-SLC7A11 regulatory circuitry contributes to cancer progression and redox balance in human hepatocarcinoma (RNA-Seq)

PROVIDER: PRJNA1032571 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26536469.fastq.gz	Fastqsanger.gz
	SRR26536470.fastq.gz	Fastqsanger.gz
	SRR26536471.fastq.gz	Fastqsanger.gz
	SRR26536472.fastq.gz	Fastqsanger.gz
	SRR26536473.fastq.gz	Fastqsanger.gz

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A novel MYC-ZNF706-SLC7A11 regulatory circuitry contributes to cancer progression and redox balance in human hepatocarcinoma (ChIP-Seq)

Project description:ZNF706 belongs to a member of C2H2-type zinc finger proteins which exerts pivotal roles in cancer progression. However, the biological function and mechanism of ZNF706 are rarely investigated. Using qRT-PCR and Western blot assays, we identified ZNF706 was frequently amplified in human hepatocarcinoma and high ZNF706 expression was associated with unfavorable HCC patient survival based on TCGA database. In vitro and in vivo experiments revealed that ZNF706 promoted HCC cell growth. Mechanistically, RNA-seq and ChIP-seq identified SLC7A11 was a critical target of ZNF706, and depletion of ZNF706 increased lipid peroxidation, cell death and decreased cystine uptake medicated by SLC7A11 contributing to redox homeostasis disruption. Furthermore, using luciferase report assays and ChIP-qPCR, we found MYC could regulate ZNF706 transcription by binding to ZNF706 promoter region, and further assay indicated MYC also involved in redox balance by modulating SLC7A11. Collectively, our study uncovers that the oncogenic role of ZNF706 in liver cancer, indicating that ZNF706 inhibition could be a potential treatment strategy for liver cancer.

2024-06-17 | GSE246331 | GEO

A novel MYC-ZNF706-SLC7A11 regulatory circuitry contributes to cancer progression and redox balance in human hepatocarcinoma (RNA-Seq)

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A novel MYC-ZNF706-SLC7A11 regulatory circuitry contributes to cancer progression and redox balance in human hepatocarcinoma

Project description:A novel MYC-ZNF706-SLC7A11 regulatory circuitry contributes to cancer progression and redox balance in human hepatocarcinoma

| PRJNA1032564 | ENA

A novel MYC-ZNF706-SLC7A11 regulatory circuitry contributes to cancer progression and redox balance in human hepatocarcinoma (ChIP-Seq)

Project description:A novel MYC-ZNF706-SLC7A11 regulatory circuitry contributes to cancer progression and redox balance in human hepatocarcinoma (ChIP-Seq)

| PRJNA1032570 | ENA

Super-enhancer-driven MLX mediates redox balance maintanance via SLC7A11 in osteosarcoma

Project description:A systematic analysis of super-enhancers identified MLX as a potential oncogene in osteosarcoma. Knockdown of MLX impaired tumor aggressiveness in vitro and in vivo, suggesting oncogenic properties of MLX. Mechanistically, silencing of MLX downregulates SLC7A11, a key gene encoding glutamate/cystine antiporter, to attenuate the uptake of cystine and interrupt the redox balance, leading to ferroptotic cell death. Pharmacological inhibition of SLC7A11 triggered massive ferroptosis and caused impaired tumor growth, providing a promising approach for osteosarcoma treatment.

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Super-enhancer-driven MLX mediates redox balance maintanance via SLC7A11 in osteosarcoma

Project description:Super-enhancer-driven MLX mediates redox balance maintanance via SLC7A11 in osteosarcoma

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A novel MYC-ZNF706-SLC7A11 regulatory circuitry contributes to cancer progression and redox balance in human hepatocarcinoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-06-17 | GSE246332 | GEO

NTRC controls chloroplast redox homeostasis through the regulation of the redox balance of 2-Cys Prxs in Arabidopsis

Project description:Thiol-dependent redox regulation is essential for the rapid adaptation of chloroplast metabolism to unpredictable changes of light intensity. The disulfide reductase activity of thioredoxins (Trxs), which relies on photo-reduced ferredoxin (Fdx) and a Fdx-dependent Trx reductase (FTR), constitutes the Fdx-FTR-Trxs system, which links chloroplast redox regulation to light. In addition, chloroplasts harbor an NADPH-dependent Trx reductase (NTR) with a joint Trx domain, NTRC. The activity of these two redox systems is integrated by the balance of the hydrogen peroxide scavenging enzyme 2-Cys peroxiredoxin (2-Cys Prx), which thus plays a key role in maintaining the reducing capacity of chloroplast Trxs in response to light intensity. Based on the severe phenotype of mutant lines lacking NTRC, it is clear that this enzyme plays an essential role in chloroplast redox homeostasis. However, whether the function of NTRC depends on its capacity of reduce 2-Cys Prxs or has additional targets remains unknown. Here, we have addressed this issue by a comparative analysis of the triple mutant of Arabidopsis thaliana, ntrc-2cpab, simultaneously lacking 2-Cys Prxs and NTRC, and the double mutant 2cpab lacking 2-Cys Prxs. The phenotype of the ntrc-2cpab mutant is indistinguishable of the 2cpab mutant, as shown by growth rate, photosynthesis performance, light-dependent redox regulation of enzyme activity and comparative transcriptomics based RNA-Seq. Based on these results, we propose that the function of NTRC in chloroplast redox homeostasis is exerted by the regulation of the redox balance of 2-Cys Prxs rather than by the direct reduction of additional targets.

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Mutant p53 mediates sensitivity to cancer treatment agents in oesophageal adenocarcinoma associated with microRNA and SLC7A11 expression

Project description:1) Background: TP53 gene mutations occur in 70% of oesophageal adenocarcinomas (OACs). Given the central role of p53 in controlling cellular response to therapy we investigated the role of mutant (mut-) p53 and SLC7A11 in a CRISPR-mediated JH-EsoAd1 TP53 knockout model. (2) Methods: Response to 2 Gy irradiation, cisplatin, 5-FU, 4-hydroxytamoxifen and endoxifen was assessed, followed by a TaqMan OpenArray qPCR screening for differences in miRNA expression. (3) Results: Knockout of mut-p53 resulted in increased chemo- and radioresistance (2 Gy survival fraction: 38% vs. 56%, p<0.0001) and in altered miRNA expression levels. Target mRNA pathways analyses indicated several potential mechanisms of treatment resistance. SLC7A11 knockdown restored radiosensitivity (2 Gy SF: 46% vs. 73%; p=0.0239), possibly via enhanced sensitivity to oxidative stress. Pathway analysis of the predicted mRNA targets of differentially expressed miRNAs indicated potential involvement in several pathways associated with apoptosis, ribosomes as well as in p53 signalling pathways. (4) Discussion: These results provide a better understanding of the important role of SLC7A11 in cancer metabolism and redox balance and the influence of p53 on these processes. Inhibition of the SLC7A11-gluthatione axis may represent a promising approach to overcome resistance associated with mut-p53.

2021-05-31 | GSE171965 | GEO

Anakinra restores cellular proteostasis by coupling mitochondrial redox balance to autophagy

Project description:Anakinra restores cellular proteostasis by coupling mitochondrial redox balance to autophagy

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