ArticleCell death & disease2017
CITED2 affects leukemic cell survival by interfering with p53 activation.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Exploring the Role of Macrophage Marker CD68 in Pediatric Acute Myeloid Leukemia.International journal of molecular sciences · 2026Article
- Resistance of E2F4DN to p38Scientific reports · 2026Article
- Article
- Potential utility of PPARγ agonists in targeting chronic myeloid leukemia stem cells.Annals of hematology · 2026Article
- CITED Proteins in Cardiac Development and Lifelong Heart Function.Journal of personalized medicine · 2025Review
- Super-Enhancer Target Gene CBP/p300-Interacting Transactivator With Glu/Asp-Rich C-Terminal Domain, 2 Cooperates With Transcription Factor Forkhead Box J3 to Inhibit Pulmonary Vascular Remodeling.Cell proliferation · 2025Article
- CXCL12 chemokine dimer signaling modulates acute myelogenous leukemia cell migration through altered receptor internalization.Scientific reports · 2025Article
- Targeting Cellular Senescence to Enhance Human Endometrial Stromal Cell Decidualization and Inhibit Their Migration.Biomolecules · 2025Article
- Review
- Evaluation of Methylation and Changes in the Transcriptomics and Proteomics of the GRHL3, PHLDA3, and in Patients with Head and Neck Squamous Cell Carcinoma.Indian journal of otolaryngology and head and neck surgery : official publication of the Association of Otolaryngologists of India · 2025Article
- In vivo genome-wide CRISPR screening identifies CITED2 as a driver of prostate cancer bone metastasis.Oncogene · 2024Article
- Cited2 inhibited hypoxia-induced proliferation and migration of PASMCs via the TGF-β1/Cited2/PPARγ pathway.Iranian journal of basic medical sciences · 2024Article
- Exploring the role of CITED transcriptional regulators in the control of macrophage polarization.Frontiers in immunology · 2024Review
- Article
- CIGB-300-Regulated Proteome Reveals Common and Tailored Response Patterns of AML Cells to CK2 Inhibition.Frontiers in molecular biosciences · 2022Article
- Role of CITED2 in stem cells and cancer.Oncology letters · 2020Review
- CITED2 and the modulation of the hypoxic response in cancer.World journal of clinical oncology · 2020Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CITED2 (CBP/p300-interacting-transactivator-with-an-ED-rich-tail 2) is a regulator of the acetyltransferase CBP/p300 and elevated CITED2 levels are shown in a number of acute myeloid leukemia (AML). To study the in vivo role of CITED2 in AML maintenance, AML cells were transduced with a lentiviral construct for RNAi-mediated knockdown of CITED2. Mice transplanted with CITED2-knockdown AML cells (n=4) had a significantly longer survival compared to mice transplanted with control AML cells (P<0.02). In vitro, the reduction of CITED2 resulted in increased p53-mediated apoptosis and CDKN1A expression, whereas BCL2 levels were reduced. The activation of p53 upon CITED2 knockdown is not a direct consequence of increased CBP/p300-activity towards p53, since no increased formation of CBP/p300/p53 complexes was demonstrated and inhibition of CBP/p300-activity could not rescue the phenotype of CITED2-deficient cells. Instead, loss of CITED2 had an inhibitory effect on the AKT-signaling pathway, which was indicated by decreased levels of phosphorylated AKT and altered expression of the AKT-pathway regulators PHLDA3 and SOX4. Notably, simultaneous upregulation of BCL2 or downregulation of the p53-target gene PHLDA3 rescued the apoptotic phenotype in CITED2-knockdown cells. Furthermore, knockdown of CITED2 led to a decreased interaction of p53 with its inhibitor MDM2, which results in increased amounts of total p53 protein. In summary, our data indicate that CITED2 functions in pathways regulating p53 activity and therefore represents an interesting target for AML therapy, since de novo AML cases are characterized by an inactivation of the p53 pathway or deregulation of apoptosis-related genes.
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Registered trials
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