ArticleNature communications2015
EZH2-mediated loss of miR-622 determines CXCR4 activation in hepatocellular carcinoma.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 77 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
77 citing papers in PubMed, 136 citations in OpenAlex.
- AMD3100 modulates the secretome responses of human Mesenchymal Stromal Cells but not their inhibitory effect on T cell proliferation.Scientific reports · 2026Article
- Study on the regulation of Treg cell infiltration by EZH2 through CXCR4/CXCL12 in diffuse large B-cell lymphoma.Clinical and experimental medicine · 2025Article
- Integrating Inflammatory and Epigenetic Signatures in IBD-Associated Colorectal Carcinogenesis: Models, Mechanisms, and Clinical Implications.International journal of molecular sciences · 2025Review
- Immunometabolic Targets in CD8Liver cancer · 2025Review
- Sublytic Activity of a Pore-Forming Protein From Commensal Bacteria Causes Epigenetic Modulation of Tumour-Affiliated Protein Expression.Journal of extracellular vesicles · 2025Article
- The epigenetic basis of hepatocellular carcinoma - mechanisms and potential directions for biomarkers and therapeutics.British journal of cancer · 2025Review
- Review
- Dual targeting of CXCR4 and EZH2 in endometriosis.iScience · 2025Article
- PA/MR imaging-guided precision phototherapy and efficacy evaluation of hepatocellular carcinoma utilizing a targeted multifunctional nanoprobe.Frontiers in immunology · 2025Article
- Oral and intratumoral microbiota influence tumor immunity and patient survival.Frontiers in immunology · 2025Article
- Transcription factor EB reprograms branched-chain amino acid metabolism and promotes pancreatic cancer progression via transcriptional regulation of BCAT1.Cell proliferation · 2024Article
- Medaka liver developed Human NAFLD-NASH transcriptional signatures in response to ancestral bisphenol A exposure.Research square · 2024Article
- Sex-specific expression of the human NAFLD-NASH transcriptional signatures in the liver of medaka with a history of ancestral bisphenol A exposure.bioRxiv : the preprint server for biology · 2024Article
- Article
- microRNA-622 upregulates cell cycle process by targeting FOLR2 to promote CRC proliferation.BMC cancer · 2024Article
- Microbiome in Cancer Development and Treatment.Microorganisms · 2023Review
- EZH2 in hepatocellular carcinoma: progression, immunity, and potential targeting therapies.Experimental hematology & oncology · 2023Review
- Review
- Preoperative systemic immune-inflammation index for predicting the prognosis of thymoma with radical resection.Thoracic cancer · 2023Article
- Hsa-circ-0006091 modulates the proliferation of hepatocellular carcinoma via the miR-622/CCNB1 axis.Turkish journal of medical sciences · 2023Article
17 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The CXC chemokine receptor 4 (CXCR4) exerts a variety of functions at different steps of hepatocellular carcinoma (HCC) progression. The molecular mechanisms and therapeutic value of CXCR4 in the development of HCC remain undefined. Here we show that aberrant CXCR4 overexpression is associated with poor prognosis and aggressive characteristics of HCC. Suppression of CXCR4 activity via CXCR4 knockdown, AMD3100 or neutralizing antibody administration inhibits hepatoma cell tumorigenesis in vitro and in vivo. CXCR4 overexpression displays the opposite effects. Using Mir library screening we identify miR-622 as a regulator of CXCR4. Further studies show that miR-622 directly target the 3' untranslated region of CXCR4 and is transcriptionally repressed by EZH2-induced H3K27 trimethylation and promoter methylation. EZH2/miR-622 promotes tumorigenesis through CXCR4. EZH2-mediated loss of miR-622 is found to correlate with CXCR4 overexpression and unfavourable prognosis in HCC patients. This study establishes EZH2/miR-622/CXCR4 as a potential adverse prognostic factor and therapeutic target for HCC patients.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.