Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Oncogenic zinc finger protein ZNF322A promotes lung cancer stemness through transcriptionally suppressing c-Myc expression [ChIP-Seq]

ABSTRACT: ZNF322A, a C2H2 zinc finger transcription factor, is an oncoprotein in lung cancer. However, the transcription mechanisms of ZNF322A in lung cancer stemness remain elusive. By integrating our chromatin immunoprecipitation-sequencing and RNA-sequencing datasets, we identified and validated transcriptional targets of ZNF322A, which significantly enriched in developmental processes. Indeed, overexpression of ZNF322A promoted self-renewal ability and increased stemness-related gene expressions in vitro and in vivo. Importantly, ZNF322A bound directly to c-Myc promoter to transcriptionally suppress c-Myc expression, which in turn increased mitochondrial oxidative phosphorylation, promoted cell motility and thus maintained lung cancer stemness properties. Clinically, ZNF322AHigh/c-MycLow expression profile was revealed as an independent factor for poor outcome of lung cancer patients. Our study provides first evidence that ZNF322A-centered transcriptome promotes lung tumorigenesis and ZNF322A acts as a transcription suppressor of c-Myc to maintain lung cancer stemness by shifting metabolism phenotype to oxidative phosphorylation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE94656 | GEO | 2019/09/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Oncogenic zinc finger protein ZNF322A promotes lung cancer stemness through transcriptionally suppressing c-Myc expression [RNA-Seq]

Project description:ZNF322A, a C2H2 zinc finger transcription factor, is an oncoprotein in lung cancer. However, the transcription mechanisms of ZNF322A in lung cancer stemness remain elusive. By integrating our chromatin immunoprecipitation-sequencing and RNA-sequencing datasets, we identified and validated transcriptional targets of ZNF322A, which significantly enriched in developmental processes. Indeed, overexpression of ZNF322A promoted self-renewal ability and increased stemness-related gene expressions in vitro and in vivo. Importantly, ZNF322A bound directly to c-Myc promoter to transcriptionally suppress c-Myc expression, which in turn increased mitochondrial oxidative phosphorylation, promoted cell motility and thus maintained lung cancer stemness properties. Clinically, ZNF322AHigh/c-MycLow expression profile was revealed as an independent factor for poor outcome of lung cancer patients. Our study provides first evidence that ZNF322A-centered transcriptome promotes lung tumorigenesis and ZNF322A acts as a transcription suppressor of c-Myc to maintain lung cancer stemness by shifting metabolism phenotype to oxidative phosphorylation.

2019-09-25 | GSE94537 | GEO

SIAH3 is frequently epigenetically silenced in cancer and regulates mitochondrial metabolism - SIAH3 Interactomics

Project description:Of the seven in absentia homologue (SIAH) family, three members have been identified in the human genome. In contrast to the E3 ubiquitin ligase encoding SIAH1 and SIAH2, little is known on the regulation and function of SIAH3 in tumorigenesis. In this study, we reveal that SIAH3 is frequently epigenetically silenced in different cancer entities, including cutaneous melanoma, lung adenocarcinoma and head and neck cancer. Low SIAH3 levels correlate with an impaired survival of cancer patients. Additionally, induced expression of SIAH3 reduces cell proliferation. Functionally, SIAH3 negatively affects cellular metabolism by shifting cells form aerobic oxidative phosphorylation to glycolysis. SIAH3 is localized in the mitochondrion and interacts with proteins involved in mitochondrial ribosome biogenesis and translation. We also report that SIAH3 interacts with ubiquitin ligases, including SIAH1 or SIAH2, and is degraded by them. These results suggest that SIAH3 acts as an epigenetically controlled tumor suppressor by regulating cellular metabolism through the inhibition of oxidative phosphorylation.

2024-01-12 | MSV000093850 | MassIVE

SIAH3 is frequently epigenetically silenced in cancer and regulates mitochondrial metabolism - Expression Proteomics Dataset

2024-01-12 | MSV000093851 | MassIVE

Demethylzeylasteral inhibits oxidative phosphorylation complex biogenesis by targeting LRPPRC in lung cancer

Project description:Demethylzeylasteral inhibits oxidative phosphorylation complex biogenesis by targeting LRPPRC in lung cancer

| PRJNA1170897 | ENA

A novel MYC-ZNF706-SLC7A11 regulatory circuitry contributes to cancer progression and redox balance in human hepatocarcinoma (RNA-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 | GSE246330 | GEO

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

2024-06-17 | GSE246331 | GEO

Gene expression profiles of human breast cancer cell lines

Project description:Numerous epithelial-to-mesenchymal transition (EMT)-promoting transcription factors have been implicated in tumorigenesis or metastasis, as well as chemoresistance of cancer. However, the underlying mechanism mediating these processes is unclear. Here we report that Foxq1, a forkhead box-containing transcription factor and EMT-inducing gene, promotes stemness traits and chemoresistance in mammary epithelial cells. We identify Twist1, Zeb2, and PDGFRM-NM-1 and M-NM-2 as Foxq1 downstream targets using an expression profiling assay. Further studies reveal that PDGFRM-NM-1 and M-NM-2 can be directly regulated by Foxq1, or indirectly through Twist1. Knockdown of both PDGFRM-NM-1 and M-NM-2 shows more significant effects on reversing Foxq1-promoted oncogenesis in vitro and in vivo than knockdown by either PDGFRM-NM-1 or M-NM-2 alone. PDGFRM-NM-2, but not PDGFRM-NM-1, shows potent effects in reversing Foxq1-promoted stemness traits. Moreover, pharmacological inhibition or gene silencing of PDGFRs sensitize mammary epithelial cells to chemotherapeutic agents in vitro and in vivo. These findings collectively indicate PDGFRs as critical mediators underlying breast cancer tumorigenesis and chemoresistance driven by EMT promoting genes, which have potential clinical implications for cancer therapy. The purpose of these experiments is to investigate the downstream targets of several transcriptional factors including Foxq1 and IRX5. Another purpose is to compare the expression pattern between basal-like breast cancer cells including MDA-MB231, SUM159 and SUM1315.

2013-05-11 | E-GEOD-46834 | biostudies-arrayexpress

Comparison of gene expression profiles human mesenchymal stromal cells (MSC) cultured in 5% oxygen atmosphere and 19.95% oxygen

Project description:Gene expression in passage 3 human healthy donor-derived MSC that had been simultaneously cultured in 5% AND 20% oxygen were compared to determine its effects on survival and proliferation The data supported some of our findings based upon functional proteome analysis showing relative increased activity in MAPK and mTOR pathways and shifting of energy metabolism from oxidative phosphorylation to glycolysis.

2021-03-03 | GSE168055 | GEO

Plakophilin 1 enhances MYC expression to promote squamous cell lung cancer

Project description:Plakophilin 1 (PKP1) is a component of desmosomes. Although desmosome function loss has been associated with increased cell migration and pro-oncogenic activity, we previously observed PKP1 overexpression in squamous cell lung cancer (SqCLC). We developed in vitro and in vivo functional models of PKP1 gain/loss in SqCLC to explore this paradox. Greater cell dissemination but reduced cell proliferation was observed in CRISPR-Cas9 PKP1-knockout clones. PKP1 expression promoted cell proliferation, cell survival, and in vivo xenograft engraftment, and these pro-oncogenic activities were mediated by the functional relationship of PKP1 with MYC. PKP1 bound to the 5’UTR of MYC mRNA, enhancing MYC translation, and MYC bound directly to the PKP1 promoter, enhancing PKP1 transcription. We propose PKP1 as a novel oncogene in SqCLC and a post-transcriptional regulator of MYC. PKP1 may be a valuable diagnostic biomarker and potential therapeutic target for SqCLC. Importantly, PKP1 inhibition may indirectly target MYC, a primary anti-cancer target.

2020-05-10 | GSE106770 | GEO

S1PR3–G12-biased agonist ALESIA targets cancer metabolism and promotes glucose starvation [MCF-7 RNA-seq]

Project description:Cancer tissues possess less glucose than surrounding normal tissue, because cancer cells predominantly produce energy by glycolysis than oxidative phosphorylation even in the presence of an adequate oxygen supply (Warburg effect). We found a novel compound ALESIA which causes apoptosis of malignant cells at a low glucose condition from an original phenotypic screening. Identified target molecule of ALESIA was Sphingosine-1-phosphate receptor 3 (S1PR3). Being different from the natural ligand, ALESIA selectively stimulated S1PR3-G12 coupling to S1PR3 without suppression by β-arrestin recruitment and continuously promoted NO synthesis. To reduce the enhanced oxidative stress, NAPDH production through pentose-phosphate pathway and resulting consumption of glucose were promoted in ALESIA-treated cells. ALESIA therefore accelerated glucose starvation of cancer cells and preferentially killed them both in vitro and in vivo.

2021-02-08 | GSE111352 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data