ArticleApoptosis : an international journal on programmed cell death2011
Mutant p53 exhibits trivial effects on mitochondrial functions which can be reactivated by ellipticine in lymphoma cells.
Article in Apoptosis : an international journal on programmed cell death, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 41 citations in OpenAlex.
- Mutagenic impact and evolutionary influence of radiotherapy in hematologic malignancies.bioRxiv : the preprint server for biology · 2024Article
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- Transition of amyloid/mutant p53 from tumor suppressor to an oncogene and therapeutic approaches to ameliorate metastasis and cancer stemness.Cancer cell international · 2022Review
- Elevation of effective p53 expression sensitizes wild-type p53 breast cancer cells to CDK7 inhibitor THZ1.Cell communication and signaling : CCS · 2022Article
- Evaluation of Interactions of Selected Olivacine Derivatives with DNA and Topoisomerase II.International journal of molecular sciences · 2021Article
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- Constitutive Activation of DNA Damage Checkpoint Signaling Contributes to Mutant p53 Accumulation via Modulation of p53 Ubiquitination.Molecular cancer research : MCR · 2016Article
- Reactivation of wild-type and mutant p53 by tryptophanolderived oxazoloisoindolinone SLMP53-1, a novel anticancer small-molecule.Oncotarget · 2016Article
- Mitochondrial p53 phosphorylation induces Bak-mediated and caspase-independent cell death.Oncotarget · 2015Article
- CK1δ in lymphoma: gene expression and mutation analyses and validation of CK1δ kinase activity for therapeutic application.Frontiers in cell and developmental biology · 2015Article
- Article
- The anticancer drug ellipticine activated with cytochrome P450 mediates DNA damage determining its pharmacological efficiencies: studies with rats, Hepatic Cytochrome P450 Reductase Null (HRN™) mice and pure enzymes.International journal of molecular sciences · 2014Review
- MnSOD in oxidative stress response-potential regulation via mitochondrial protein influx.Antioxidants & redox signaling · 2014Review
- Chemical metabolic inhibitors for the treatment of blood-borne cancers.Anti-cancer agents in medicinal chemistry · 2014Review
- Targeting cancer cell mitochondria as a therapeutic approach.Future medicinal chemistry · 2013Review
- Article
- Deficiency of the complex I of the mitochondrial respiratory chain but improved adenylate control over succinate-dependent respiration are human gastric cancer-specific phenomena.Molecular and cellular biochemistry · 2012Article
- Review
- Oxidative Stress Induced by MnSOD-p53 Interaction: Pro- or Anti-Tumorigenic?Journal of signal transduction · 2012Article
- Enhancing mitochondrial respiration suppresses tumor promoter TPA-induced PKM2 expression and cell transformation in skin epidermal JB6 cells.Cancer prevention research (Philadelphia, Pa.) · 2011Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Increasing evidence has shown that a fraction of the wild-type (wt) form of the tumor suppressor p53, can translocate to mitochondria due to genotoxic stress. The mitochondrial targets of wt p53 have also been studied. However, whether mutant p53, which exists in 50% of human cancers, translocates to mitochondria and affects mitochondrial functions is unclear. In this study, we used doxorubicin, a chemotherapeutic drug, to treat five human lymphoma cell lines with wt, mutant or deficient in p53, to induce p53 activation and mitochondrial translocation. Our results demonstrated that mutant p53, like wt p53, was induced upon doxorubicin treatment. Similarly, a fraction of mutant p53 also translocated to mitochondria. However, Complex I and II activities in the mitochondria were compromised only in wt p53-bearing cells after doxorubicin treatment, but not in mutant p53-bearing cells. Similarly, doxorubicin treatment caused greater cell death only in wt p53-bearing cells, but not in mutant p53-bearing cells. When p53 deficient Ramos cells were transfected with mutant p53 (249S), the cells showed resistance to doxorubicin-induced cell death and decreases in complex activities. To reactivate mutant p53 and reverse chemoresistance, ellipticine (5,11-dimethyl-6H-pyrido[4,3-b]carbazole) was used to treat mutant p53 cells. Ellipticine enhanced p53 mitochondrial translocation, decreased Complex I activity, and sensitized p53 mutant cells to doxorubicin-induced apoptosis. In summary, our studies suggest that mutations in p53 may not hinder p53's mitochondrial translocation, but impair its effects on mitochondrial functions. Therefore, restoring mutant p53 by ellipticine may sensitize these cells to chemotherapy.
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