ArticleCancer biology & therapy2012
Inauhzin and Nutlin3 synergistically activate p53 and suppress tumor growth.
Article in Cancer biology & therapy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 27 citations in OpenAlex.
- SREBP2-activated CNPY3 Phase Separation Promotes Colorectal Cancer by Enhancing MDM2-mediated p53 Degradation.International journal of biological sciences · 2026Article
- Emerging role of sirtuins in non‑small cell lung cancer (Review).Oncology reports · 2024Review
- Targeting sirtuins for cancer therapy: epigenetics modifications and beyond.Theranostics · 2024Review
- Isoquercitrin protects HUVECs against high glucose‑induced apoptosis through regulating p53 proteasomal degradation.International journal of molecular medicine · 2021Article
- Metformin Inhibits the Urea Cycle and Reduces Putrescine Generation in Colorectal Cancer Cell Lines.Molecules (Basel, Switzerland) · 2021Article
- Synergistic effect of Nutlin-3 combined with MG-132 on schwannoma cells through restoration of merlin and p53 tumour suppressors.EBioMedicine · 2018Article
- Reviving the guardian of the genome: Small molecule activators of p53.Pharmacology & therapeutics · 2017Review
- Acetylation Is Crucial for p53-Mediated Ferroptosis and Tumor Suppression.Cell reports · 2016Article
- TFIIS.h, a new target of p53, regulates transcription efficiency of pro-apoptotic bax gene.Scientific reports · 2016Article
- Repositioning antipsychotic chlorpromazine for treating colorectal cancer by inhibiting sirtuin 1.Oncotarget · 2015Article
- P53 mutations in colorectal cancer - molecular pathogenesis and pharmacological reactivation.World journal of gastroenterology · 2015Review
- Inauhzin(c) inactivates c-Myc independently of p53.Cancer biology & therapy · 2015Article
- Identification of a novel polyprenylated acylphloroglucinol‑derived SIRT1 inhibitor with cancer‑specific anti-proliferative and invasion-suppressing activities.International journal of oncology · 2014Article
- Article
- Targeting p53-MDM2-MDMX loop for cancer therapy.Sub-cellular biochemistry · 2014Review
- Inauhzin sensitizes p53-dependent cytotoxicity and tumor suppression of chemotherapeutic agents.Neoplasia (New York, N.Y.) · 2013Article
- SIRT1: Regulator of p53 Deacetylation.Genes & cancer · 2013Article
- The emerging anti-proliferative role of Nutlin-3 in the pathogenesis of systemic malignancies.Cancer biology & therapy · 2013Article
- Article
- Structure and activity analysis of Inauhzin analogs as novel antitumor compounds that induce p53 and inhibit cell growth.PloS one · 2012Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Several proteins have been suggested in promoting tumor formation in numerous human tissues by inactivating the tumor suppressor p53. This has generated interest in the development of small molecules to block these inhibitors of p53 and to regain p53 activity. Recently, we identified a small molecule, Inauhzin, which can inhibit SIRT1 activity and activate p53. SIRT1 is a deacetylase that deacetylates p53 and facilitates Mdm2 mediated p53 destabilization. In this study, we tested if combining Inauhzin with Nutlin-3, an inhibitor of MDM2-p53 binding, might synergistically activate p53 to suppress tumor growth. Indeed, at lower doses, combination of Inauhzin and Nutlin-3 exhibited a synergistic effect on inhibiting cell growth and promoting apoptosis in human colon and lung cancer cell lines in a p53-dependent fashion. Minimal effects were observed with treatment of either compound alone. Using a xenograft tumor model, we also showed a synergistic effect with both compounds. Thus, to fully regain p53 activity, targeting its multiple inhibitory proteins might be a better approach. Our study provides evidence supporting this concept for achieving better therapeutic efficacy in tumors that possess wild type p53.
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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.