ZNF251 promotes the progression of lung cancer by activating ERK signaling

Zhong, Caiyun; Chen, Chunji; Yao, Feng; Fang, Wentao

doi:10.1111/cas.14547

Cited by 10 publications

(6 citation statements)

References 21 publications

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“…However, the role of ZNF251 in human physiology is currently unknown. Even so, this gene has been associated to the promotion of lung cancer through activation of the ERK signalling pathway ( 139 ). This signalling pathway is closely associated with AT biology and glucose sensitivity, so one may posit that this gene could affect the MUHO phenotype by the ERK signalling pathway ( 109 ).…”

Section: Resultsmentioning

confidence: 99%

Adipose Tissue Epigenetic Profile in Obesity-Related Dysglycemia - A Systematic Review

et al. 2021

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BackgroundObesity is a major risk factor for dysglycemic disorders, including type 2 diabetes (T2D). However, there is wide phenotypic variation in metabolic profiles. Tissue-specific epigenetic modifications could be partially accountable for the observed phenotypic variability.ScopeThe aim of this systematic review was to summarize the available data on epigenetic signatures in human adipose tissue (AT) that characterize overweight or obesity-related insulin resistance (IR) and dysglycemia states and to identify potential underlying mechanisms through the use of unbiased bioinformatics approaches.MethodsOriginal data published in the last decade concerning the comparison of epigenetic marks in human AT of individuals with metabolically unhealthy overweight/obesity (MUHO) versus normal weight individuals or individuals with metabolically healthy overweight/obesity (MHO) was assessed. Furthermore, association of these epigenetic marks with IR/dysglycemic traits, including T2D, was compiled.ResultsWe catalogued more than two thousand differentially methylated regions (DMRs; above the cut-off of 5%) in the AT of individuals with MUHO compared to individuals with MHO. These DNA methylation changes were less likely to occur around the promoter regions and were enriched at loci implicated in intracellular signaling (signal transduction mediated by small GTPases, ERK1/2 signaling and intracellular trafficking). We also identified a network of seven transcription factors that may play an important role in targeting DNA methylation changes to specific genes in the AT of subjects with MUHO, contributing to the pathogeny of obesity-related IR/T2D. Furthermore, we found differentially methylated CpG sites at 8 genes that were present in AT and whole blood, suggesting that DMRs in whole blood could be potentially used as accessible biomarkers of MUHO.ConclusionsThe overall evidence linking epigenetic alterations in key tissues such AT to metabolic complications in human obesity is still very limited, highlighting the need for further studies, particularly those focusing on epigenetic marks other than DNA methylation. Our initial analysis suggests that DNA methylation patterns can potentially discriminate between MUHO from MHO and provide new clues into why some people with obesity are less susceptible to dysglycemia. Identifying AT-specific epigenetic targets could also lead to novel approaches to modify the progression of individuals with obesity towards metabolic disease.Systematic Review RegistrationPROSPERO, identifier CRD42021227237.

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Section: Resultsmentioning

confidence: 99%

Adipose Tissue Epigenetic Profile in Obesity-Related Dysglycemia - A Systematic Review

et al. 2021

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“…The ERK signaling pathway has multiple roles in tumors, including proliferation and metastasis. , Hyperactivation of the ERK often occurs in lung cancer patients . Excessive activation of the ERK pathway promotes the malignant transformation of lung epithelial cells .…”

Section: Discussionmentioning

confidence: 99%

BIRC3–HSP90B1 Interaction Inhibits Non-Small Cell Lung Cancer Progression through the Extracellular Signal-Regulated Kinase Pathway

Suo,

Wu,

Zhou

et al. 2024

ACS Omega

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The long-term prognosis of nonsmall cell lung cancer (NSCLC) remains unsatisfactory, which is a major challenge in lung cancer treatment. BIRC3 is an inhibitor of apoptosis (IAP) protein that contributes to tumor regulation. However, the underlying regulatory mechanisms of BIRC3 in NSCLC remains unknown. We initiated an analysis of BIRC3 expression data in NSCLC tumors and adjacent tissues using the TCGA and GEO databases and examined the variations in prognosis. Further, we conducted overexpression (OE) and knockdown (KD) studies on BIRC3 to evaluate its effects on NSCLC cell proliferation, migration, and invasion. Additionally, through utilization of a nude mouse model, the regulatory effects of BIRC3 on NSCLC were verified in vivo. Co-immunoprecipitation (Co-IP) assay served to pinpoint the proteins with which BIRC3 interacts. The results indicated that BIRC3 is down-regulated in NSCLC tissues and that patients with high BIRC3 expression demonstrate a better prognosis. BIRC3 is a tumor suppressor, inhibiting the proliferation and metastasis of NSCLC. Co-IP results revealed that BIRC3 interacts with HSP90B1, leading to a decrease in HSP90B1 expression and subsequent negative regulation of the ERK signaling pathway. BIRC3 may serve as a prognostic biomarker for NSCLC. It directly interacts with HSP90B1 to negatively regulate the ERK signaling pathway, thereby hindering the progression of NSCLC.

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“…In colon cancer, wild-type protein kinase N2 (PKN2) dephosphorylates ERK1/2 by directly binding to the DUSP6 junction and increasing its the transcriptional activation of the DUSP6 gene is succeeded by ERK-stimulated DUSP6 phosphorylation that promotes its degradation and gives positive feedback phosphatase activity; ERK1/2 dephosphorylation further promotes DUSP6 activity [43]. Zinc nger protein ZNF251 directly binds to the DUSP6 promoter to negatively regulate it and activate the MAPK/ERK signaling in lung cancer [44]. Zinc nger protein ZNF251 directly binds to the DUSP6 promoter to negatively regulate it and activate the MAPK/ERK signaling in lung cancer [45].…”

Section: Discussionmentioning

confidence: 99%

YY1 promotes breast cancer metastasis via the DUSP6/p-ERK1/2 signaling axis 1

He,

Zhou,

et al. 2023

Preprint

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Background: The incidence of breast cancer (BC) and mortality from metastasis continue to increase. Yin Yang-1 (YY1) transcription factor is involved in tumor progression; however, its function in BC metastasis and its molecular mechanisms remain unclear. Methods: The expression level and prognosis of YY1 in BC were determined by bioinformatic analysis. The biological functions of YY1 were assessed on lentiviral constructs of overexpression and shRNA cell lines using wound-healing and transwell assays, and lung metastasis was observed by bioluminescence imaging of nude mice injected subcutaneously with selected cell lines. Western blotting was conducted to measure the protein levels of genes related to the extracellular signal-regulated kinase (ERK) signaling pathway and markers for the epithelial-mesenchymal transition (EMT). The binding of YY1 to the promoter of dual specificity phosphatase 6 (DUSP6) was evaluated by means of a luciferase reporter gene assay. Results: In BC tissues, YY1 is expressed at a high level, and a higher expression level of YY1 is linked to the N and M stages and a worse prognosis. YY1 promotes the invasion, migration, and EMT of BC cells both in vitro and in vivo. This is the first study of BC to show how YY1 binds to the DUSP6 promoter and represses its transcription, thus activating the ERK pathway to promote EMT and BC progression. Conclusions: As an oncogene, YY1 promotes BC metastasis by targeting DUSP6 to activate the ERK pathway. For patients with BC, it could serve as a novel treatment target.

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ZNF251 promotes the progression of lung cancer by activating ERK signaling

Cited by 10 publications

References 21 publications

Adipose Tissue Epigenetic Profile in Obesity-Related Dysglycemia - A Systematic Review

Adipose Tissue Epigenetic Profile in Obesity-Related Dysglycemia - A Systematic Review

BIRC3–HSP90B1 Interaction Inhibits Non-Small Cell Lung Cancer Progression through the Extracellular Signal-Regulated Kinase Pathway

YY1 promotes breast cancer metastasis via the DUSP6/p-ERK1/2 signaling axis 1

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