ArticleNature communications2016
Histone variant H3F3A promotes lung cancer cell migration through intronic regulation.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- Germline variants and breast cancer survival in patients with distant metastases at primary breast cancer diagnosis.Scientific reports · 2021Pooled it
- Histone variant H2A.J is an epigenetic regulator of metastasis in lung adenocarcinoma.Cell death & disease · 2026Article
- Double jeopardy: howFrontiers in cell and developmental biology · 2026Review
- Near Infrared Photoimmunotherapy for Lung Cancer: Recent Development and Perspective.ImmunoTargets and therapy · 2026Review
- Comprehensive Genomic Profiling of Small-Cell Lung Cancer Reveals Frequent Potentially Targetable Alterations.International journal of molecular sciences · 2025Article
- Implications of canonical histone H3.1 and histone variant H3.3 in cancer.Open biology · 2025Review
- The path of GPR87: from a P2Y-like receptor to its role in cancer progression.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Exogenous expression of a histone H3.3 isoform causes extranuclear divisions in thebioRxiv : the preprint server for biology · 2025Article
- Roles of Histone H2B, H3 and H4 Variants in Cancer Development and Prognosis.International journal of molecular sciences · 2024Review
- Article
- Knockout tales: the versatile roles of histone H3.3 in development and disease.Epigenetics & chromatin · 2023Review
- Involvement of the H3.3 Histone Variant in the Epigenetic Regulation of Gene Expression in the Nervous System, in Both Physiological and Pathological Conditions.International journal of molecular sciences · 2023Review
- Differential effect of histone H3.3 depletion on retroviral repression in embryonic stem cells.Clinical epigenetics · 2023Article
- Darinaparsin (ZIO-101) enhances the sensitivity of small-cell lung cancer to PARP inhibitors.Acta pharmacologica Sinica · 2023Article
- Genetic and epigenetic regulation of the NRF2-KEAP1 pathway in human lung cancer.British journal of cancer · 2022Review
- Histone variants: The unsung guardians of the genome.DNA repair · 2022Review
- The Current State of Chromatin Immunoprecipitation (ChIP) from FFPE Tissues.International journal of molecular sciences · 2022Review
- Article
- Adipocyte-mediated epigenomic instability in human T-ALL cells is cytotoxic and phenocopied by epigenetic-modifying drugs.Frontiers in cell and developmental biology · 2022Article
- The dark side of histones: genomic organization and role of oncohistones in cancer.Clinical epigenetics · 2021Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although several somatic single nucleotide variations in histone H3.3 have been investigated as cancer drivers, other types of aberration have not been well studied. Here, we demonstrate that overexpression of H3F3A, encoding H3.3, is associated with lung cancer progression and promotes lung cancer cell migration by activating metastasis-related genes. H3.3 globally activates gene expression through the occupation of intronic regions in lung cancer cells. Moreover, H3.3 binding regions show characteristics of regulatory DNA elements. We show that H3.3 is deposited at a specific intronic region of GPR87, where it modifies the chromatin status and directly activates GPR87 transcription. The expression levels of H3F3A and GPR87, either alone or in combination, are robust prognostic markers for early-stage lung cancer, and may indicate potential for the development of treatments involving GPR87 antagonists. In summary, our results demonstrate that intronic regulation by H3F3A may be a target for the development of novel therapeutic strategies.
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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.