ArticleOncotarget2014
Nuclear and cytoplasmic p53 suppress cell invasion by inhibiting respiratory complex-I activity via Bcl-2 family proteins.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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
28 citing papers in PubMed, 48 citations in OpenAlex.
- Mitochondrially Targeted p53-Bad* Fusion Gene Therapy Promotes Apoptosis in Hepatocellular Carcinoma by Pan-Bcl-2 Inhibition.Molecular pharmaceutics · 2025Article
- Mitochondrial PTRH2 controls the deubiquitinase TRABID to regulate mt-ND5 stability and metabolism.PNAS nexus · 2025Article
- TPepPro: a deep learning model for predicting peptide-protein interactions.Bioinformatics (Oxford, England) · 2024Article
- Cell-specific modulation of mitochondrial respiration and metabolism by the pro-apoptotic Bcl-2 family members Bax and Bak.Apoptosis : an international journal on programmed cell death · 2024Article
- Chemotherapy induces cell plasticity; controlling plasticity increases therapeutic response.Signal transduction and targeted therapy · 2023Article
- An integrative systems biology approach to overcome venetoclax resistance in acute myeloid leukemia.PLoS computational biology · 2022Article
- Mitochondrial inhibitors circumvent adaptive resistance to venetoclax and cytarabine combination therapy in acute myeloid leukemia.Nature cancer · 2021Article
- Slug promotes p53 and p21 protein degradation by inducing Mdm2 expression in HCT116 colon cancer cells.Oncology letters · 2021Article
- A mitochondrial journey through acetaminophen hepatotoxicity.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2020Review
- BCL-w: apoptotic and non-apoptotic role in health and disease.Cell death & disease · 2020Review
- Photobiomodulation Mediates Neuroprotection against Blue Light Induced Retinal Photoreceptor Degeneration.International journal of molecular sciences · 2020Article
- The role of oxidative stress-mediated apoptosis in the pathogenesis of uric acid nephropathy.Renal failure · 2019Article
- p53-Bad: A Novel Tumor Suppressor/Proapoptotic Factor Hybrid Directed to the Mitochondria for Ovarian Cancer Gene Therapy.Molecular pharmaceutics · 2019Article
- Dissecting the expression landscape of mitochondrial genes in lung squamous cell carcinoma and lung adenocarcinoma.Oncology letters · 2018Article
- Novel Mitochondria-Targeted Furocoumarin Derivatives as Possible Anti-Cancer Agents.Frontiers in oncology · 2018Article
- Oncogenic Metabolism Acts as a Prerequisite Step for Induction of Cancer Metastasis and Cancer Stem Cell Phenotype.Oxidative medicine and cellular longevity · 2018Review
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- Selective Disruption of Respiratory Supercomplexes as a New Strategy to Suppress Her2Antioxidants & redox signaling · 2017Article
- HOXA5 and p53 cooperate to suppress lung cancer cell invasion and serve as good prognostic factors in non-small cell lung cancer.Journal of Cancer · 2017Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Although the p53 tumor suppressor/transcription factor often accumulates in the cytoplasm of healthy cells, limited information is available on the cytoplasmic function of p53. Here, we show that cytoplasmic p53 suppresses cell invasion by reducing mitochondrial reactive oxygen species (ROS) levels. Analysis revealed that this function is mediated by Bcl-2 family proteins: Cytoplasmic p53 binds Bcl-w, liberating Bax, which then binds ND5, a subunit of respiratory complex-I, thereby suppressing complex-I activity and thus ROS production. The G13289A mutation of ND5, identified in cancer patients, prevents Bax/ND5 interactions and promotes ROS production and cell invasion. We also showed that Bcl-XL and Bak can substitute for Bcl-w and Bax, respectively, regulating complex-I activity and supporting the cytoplasmic function of p53; nuclear p53 also suppresses complex-I activity by inducing Bax expression. Studies in animal models support the notion that p53 and Bcl-2 family proteins exhibit these functions in vivo. This study demonstrates a link between p53 and Bcl-2 proteins as regulators of ROS production and cellular invasiveness, and reveals complex-I, especially ND5, as their functional target.
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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.