ArticleThe Journal of biological chemistry2012
Oncogene Ras/phosphatidylinositol 3-kinase signaling targets histone H3 acetylation at lysine 56.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 51 citations in OpenAlex.
- The DNA damage-independent ATM signalling maintains CBP/DOT1L axis in MLL rearranged acute myeloid leukaemia.Oncogene · 2024Article
- Chromatin modifiers in human disease: from functional roles to regulatory mechanisms.Molecular biomedicine · 2024Review
- Genetic inhibitors of APOBEC3B-induced mutagenesis.Genome research · 2023Article
- Oncogenic signaling-mediated regulation of chromatin during tumorigenesis.Cancer metastasis reviews · 2023Review
- Review
- Incorporation of a histone mutant with H3K56 site substitution perturbs the replication machinery in mouse embryonic stem cells.Journal of molecular cell biology · 2022Article
- Histone H3 deacetylation promotes host cell viability for efficient infection by Listeria monocytogenes.PLoS pathogens · 2021Article
- Molecular dynamics simulations reveal how H3K56 acetylation impacts nucleosome structure to promote DNA exposure for lesion sensing.DNA repair · 2021Article
- The impact of CBP expression in estrogen receptor-positive breast cancer.Clinical epigenetics · 2021Article
- Histone Modifications and their Role in Colorectal Cancer (Review).Pathology oncology research : POR · 2020Review
- The Ras-ERK signaling pathway regulates acetylated activating transcription factor 2 via p300 in pancreatic cancer cells.Annals of translational medicine · 2020Article
- Article
- Forcing ATGL expression in hepatocarcinoma cells imposes glycolytic rewiring through PPAR-α/p300-mediated acetylation of p53.Oncogene · 2019Article
- Epigenetic changes during aging and their reprogramming potential.Critical reviews in biochemistry and molecular biology · 2019Review
- Article
- Ras-ERK1/2 Signaling Promotes The Development Of Osteosarcoma By Regulating H2BK12ac Through CBP.Cancer management and research · 2019Article
- USP52 acts as a deubiquitinase and promotes histone chaperone ASF1A stabilization.Nature communications · 2018Article
- Oncogenic N-Ras Stimulates SRF-Mediated Transactivation via H3 Acetylation at Lysine 9.BioMed research international · 2018Article
- Regulation of stem cell aging by SIRT1 - Linking metabolic signaling to epigenetic modifications.Molecular and cellular endocrinology · 2017Review
- Human Amniocytes Are Receptive to Chemically Induced Reprogramming to Pluripotency.Molecular therapy : the journal of the American Society of Gene Therapy · 2017Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is well established that the small GTPase Ras promotes tumor initiation by activating at least three different mediators: Raf, PI3K, and Ras-like (Ral) guanine nucleotide exchange factors. However, the exact mechanisms that underlie these different Ras signaling pathways, which are involved in tumor progression, remain to be elucidated. In this study, we report that the Ras-PI3K pathway, but not Raf or the Ral guanine nucleotide exchange factors, specifically targets the acetylation of H3 at lysine 56 (H3K56ac), thereby regulating tumor cell activity. We demonstrate that the Ras-PI3K-induced reduction in H3K56ac is associated with the proliferation and migration of tumor cells by targeting the transcription of tumor-associated genes. The depletion of the histone deacetyltransferases Sirt1 and Sirt2 rescues the Ras-PI3K-induced decrease in H3K56ac, gene transcription, tumor cell proliferation, and tumor cell migration. Furthermore, we demonstrate that the Ras-PI3K-AKT pathway regulates H3K56ac via the MDM2-dependent degradation of CREB-binding protein/p300. Taken together, the results of this study demonstrate that the Ras-PI3K signaling pathway targets specific epigenetic modifications in tumor cells.
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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.