ArticleOncotarget2016
Downregulation of ATOH8 induced by EBV-encoded LMP1 contributes to the malignant phenotype of nasopharyngeal carcinoma.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- Role of ATOH8 in Mitigating Cardiac Fibrosis in Heart Failure via Inhibition of the Transcriptional Repression of Smad7 by RUNX2.Biomolecules & therapeutics · 2026Article
- Loss of Atoh8 Impairs Macroautophagy.Cells · 2025Article
- "Friends or foes": a new perspective of tumour metabolic transcriptional modification.Cell death & disease · 2025Review
- FXR1 associates with and degrades PDZK1IP1 and ATOH8 mRNAs and promotes esophageal cancer progression.Biology direct · 2024Article
- Resveratrol Inhibits Nasopharyngeal Carcinoma (NPC) by Targeting the MAPK Signaling Pathway.Anti-cancer agents in medicinal chemistry · 2024Article
- Atoh8 in Development and Disease.Biology · 2022Review
- Mitochondria dysfunction in circulating tumor cells.Frontiers in oncology · 2022Review
- Atonal homolog 8/Math6 regulates differentiation and maintenance of skeletal muscle.Frontiers in cell and developmental biology · 2022Article
- Targeted deletion of Atoh8 results in severe hearing loss in mice.Genesis (New York, N.Y. : 2000) · 2021Article
- A novel isoform of ATOH8 promotes the metastasis of breast cancer by regulating RhoC.Journal of molecular cell biology · 2021Article
- Shear stress activates ATOH8 via autocrine VEGF promoting glycolysis dependent-survival of colorectal cancer cells in the circulation.Journal of experimental & clinical cancer research : CR · 2020Article
- ATOH8 overexpression inhibits the tumor progression and monocyte chemotaxis in hepatocellular carcinoma.International journal of clinical and experimental pathology · 2020Article
- CYP3A5 suppresses metastasis of lung adenocarcinoma through ATOH8/Smad1 axis.American journal of cancer research · 2020Article
- Genome-wide association study of circulating folate one-carbon metabolites.Genetic epidemiology · 2019Article
- Integrated transcriptomics reveals master regulators of lung adenocarcinoma and novel repositioning of drug candidates.Cancer medicine · 2019Article
- Article
- Quantitation of DNA methylation in Epstein-Barr virus-associated nasopharyngeal carcinoma by bisulfite amplicon sequencing.BMC cancer · 2017Article
- Comprehensive tissue-specific gene set enrichment analysis and transcription factor analysis of breast cancer by integrating 14 gene expression datasets.Oncotarget · 2017Article
- Role of Epstein-Barr Virus in the Development of Nasopharyngeal Carcinoma.Open medicine (Warsaw, Poland) · 2017Article
- In vivo and in vitro study of co-expression of LMP1 and Cripto-1 in nasopharyngeal carcinoma.Brazilian journal of otorhinolaryngologyArticle
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mechanism for the malignant phenotype of nasopharyngeal carcinoma (NPC) remains poorly understood. Epstein-Barr virus (EBV) consistently appears in nearly all malignant NPC patient samples, suggesting the strong etiological link between the malignant phenotype and EBV infection. Here we found that the EBV-encoded latent membrane protein (LMP1) enhanced cell growth, motility, invasion and xenograft tumor growth of NPC. RNA-seq profiling analysis of LMP1-positive NPC patient tissues indicated that widespread gene repression contributed to malignant phenotype of NPC. The transcription factor binding site (TFBS) enrichment analysis indicated a subset of transcription factors including ATOH8, a novel transcript factor which belongs to the basic helix-loop-helix (bHLH) gene family inversely enriched in promoters of up-regulated genes and down-regulated genes. Importantly, the expression of ATOH8 was suppressed in both immortalized normal nasopharyngeal epithelial cells (NPEC) and NPC cells with LMP1 overexpression. The Real-Time PCR and Western Blot assays indicated that ATOH8 decreased expression in NPC cell lines and patient samples. Moreover, by gain- or loss-of-function assays, we demonstrated that ATOH8 inhibition promoted malignant phenotype, whereas ATOH8 restoration reversed malignant phenotype of NPC. Finally, we demonstrated that LMP1 inhibited ATOH8 expression by epigenetically impairing the occupancy of activating H3K4me3 and enhancing the occupancy of repressive H3K27me3 on ATOH8 promoter. Collectively, our study uncovered the occurrence of malignant phenotype of NPC induced by EBV infection and characterized a novel bHLH transcription factor ATOH8 as a new downstream target of LMP1.
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