ArticleInternational journal of molecular medicine2018
c-Myc regulates the CDK1/cyclin B1 dependent‑G2/M cell cycle progression by histone H4 acetylation in Raji cells.
Article in International journal of molecular medicine, 2018. 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 37 papers.
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37 citing papers in PubMed, 45 citations in OpenAlex.
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- A Knock-In Mouse Model of Thymoma With the GTF2I L424H Mutation.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2022Article
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- p53 deficiency promotes bone regeneration by functional regulation of mesenchymal stromal cells and osteoblasts.Journal of bone and mineral metabolism · 2022Article
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- DEPDC1B promotes development of cholangiocarcinoma through enhancing the stability of CDK1 and regulating malignant phenotypes.Frontiers in oncology · 2022Article
- Ailanthone Inhibits Cell Proliferation in Tongue Squamous Cell Carcinoma via PI3K/AKT Pathway.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Radiosensitizing Effect of Celastrol by Inhibiting G2/M Phase Arrest Induced by the c-myc Gene of Human SW1353 Chondrosarcoma Cells: Network and Experimental Analyses.BioMed research international · 2022Article
- P38 MAPK/AKT signalling is involved in IL-33-mediated anti-apoptosis in childhood acute lymphoblastic leukaemia blast cells.Annals of medicine · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Overexpression of c-Myc is involved in the tumorigenesis of B-lineage acute lymphoblastic leukemia (B‑ALL), but the mechanism is not well understood. In the present study, a c‑Myc‑knockdown model (Raji‑KD) was established using Raji cells, and it was indicated that c‑Myc regulates the expression of genes associated with cell cycle progression in G2/M‑phase, cyclin D kinase (CDK)1 and cyclin B1, by modulating 60 kDa Tat‑interactive protein (TIP60)/males absent on the first (MOF)‑mediated histone H4 acetylation (AcH4), which was then completely restored by re‑introduction of the c‑Myc gene into the Raji‑KD cells. The expression of CDK1 and cyclin B1 was markedly suppressed in Raji‑KD cells, resulting in G2/M arrest. In comparison to Raji cells, the proliferation of Raji‑KD cells was significantly reduced, and it was recovered via re‑introduction of the c‑Myc gene. In the tumorigenesis assays, the loss of c‑Myc expression significantly suppressed Raji cell‑derived lymphoblastic tumor formation. Although c‑Myc also promotes Raji cell apoptosis via the caspase‑3‑associated pathway, CDK1/cyclin B1‑dependent‑G2/M cell cycle progression remains the major driving force of c‑Myc‑controlled tumorigenesis. The present results suggested that c‑Myc regulates cyclin B1‑ and CDK1‑dependent G2/M cell cycle progression by TIP60/MOF-mediated AcH4 in Raji cells.
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