ReviewOncotarget2015
Reactivating p53 functions by suppressing its novel inhibitor iASPP: a potential therapeutic opportunity in p53 wild-type tumors.
Review in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The trial behind it
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.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- Comprehensive bioinformatics analysis and clinical validation of PPP1R13L in rectal adenocarcinoma.BMC cancer · 2026Article
- Regulation of immunological tolerance by the p53-inhibitor iASPP.Cell death & disease · 2023Article
- Erb‑B2 Receptor Tyrosine Kinase 2 is negatively regulated by the p53‑responsive microRNA‑3184‑5p in cervical cancer cells.Oncology reports · 2021Observational
- Emerging role of F-box proteins in the regulation of epithelial-mesenchymal transition and stem cells in human cancers.Stem cell research & therapy · 2019Review
- The anti-apoptotic proteins NAF-1 and iASPP interact to drive apoptosis in cancer cells.Chemical science · 2019Article
- P21 and P27 promote tumorigenesis and progression via cell cycle acceleration in seminal vesicles of TRAMP mice.International journal of biological sciences · 2019Article
- Mild Therapeutic Hypothermia Protects the Brain from Ischemia/Reperfusion Injury through Upregulation of iASPP.Aging and disease · 2018Article
- Role of Kruppel-like factor 4 in regulating inhibitor of apoptosis-stimulating protein of p53 in the progression of gastric cancer.Oncology letters · 2018Article
- Deficiency of protein-L-isoaspartate (D-aspartate)Oncotarget · 2018Article
- 2-anilino-4-amino-5-aroylthiazole-type compound AS7128 inhibits lung cancer growth through decreased iASPP and p53 interaction.Cancer science · 2018Article
- B7H3 As a Promoter of Metastasis and Promising Therapeutic Target.Frontiers in oncology · 2018Review
- P53-derived hybrid peptides induce apoptosis of synovial fibroblasts in the rheumatoid joint.Oncotarget · 2017Article
- Sertad1 antagonizes iASPP function by hindering its entrance into nuclei to interact with P53 in leukemic cells.BMC cancer · 2017Article
- Musashi-2, a novel oncoprotein promoting cervical cancer cell growth and invasion, is negatively regulated by p53-induced miR-143 and miR-107 activation.Journal of experimental & clinical cancer research : CR · 2017Article
- Wild-type and mutant p53 differentially modulate miR-124/iASPP feedback following pohotodynamic therapy in human colon cancer cell line.Cell death & disease · 2017Article
- CDK1 interacts with iASPP to regulate colorectal cancer cell proliferation through p53 pathway.Oncotarget · 2017Article
- iASPP induces EMT and cisplatin resistance in human cervical cancer through miR-20a-FBXL5/BTG3 signaling.Journal of experimental & clinical cancer research : CR · 2017Article
- Suppression of iASPP-dependent aggressiveness in cervical cancer through reversal of methylation silencing of microRNA-124.Scientific reports · 2016Article
- Inhibition of WIP1 phosphatase sensitizes breast cancer cells to genotoxic stress and to MDM2 antagonist nutlin-3.Oncotarget · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although mutational inactivation of p53 is found in 50% of all human tumors, a subset of tumors display defective p53 function, but retain wild-type (WT) p53. Here, direct and indirect mechanisms leading to the loss of WT p53 activities are discussed. We summarize the oncogenic roles of iASPP, an inhibitor of WT p53, in promoting proliferation, invasion, drug or radiation-resistance and metastasis. From the therapeutic view, we highlight promising perspectives of microRNA-124, peptide and small molecules that reduce or block iASPP for the treatment of cancer. High iASPP expression enhances proliferation, aggressive behavior, the resistance to radiation/chemotherapy and correlates with poor prognosis in a range of human tumors. Overexpression of iASPP accelerates tumorigenesis and invasion through p53-dependent and p53-independent mechanisms. MicroRNA-124 directly targets iASPP and represses the growth and invasiveness of cancer cells. The disruption of iASPP-p53 interaction by a p53-derived peptide A34 restores p53 function in cancer cells. The inhibition of iASPP phosphorylation with small molecules induces p53-dependent apoptosis and growth suppression. The mechanisms underlying aberrant expression of iASPP in human tumors should be further investigated. Reactivating WT p53 functions by targeting its novel inhibitor iASPP holds promise for potential therapeutic interventions in the treatment of WT p53-containing tumors.
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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.