ArticleAging2010
Phospho-ΔNp63α/Rpn13-dependent regulation of LKB1 degradation modulates autophagy in cancer cells.
Article in Aging, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
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, 28 citations in OpenAlex.
- Bioactive Compounds with Antiglioma Activity from Marine Species.Biomedicines · 2021Review
- Neural suppression of miRNA-181a in the kidney elevates renin expression and exacerbates hypertension in Schlager mice.Hypertension research : official journal of the Japanese Society of Hypertension · 2020Article
- Article
- Autophagic Mechanism in Anti-Cancer Immunity: Its Pros and Cons for Cancer Therapy.International journal of molecular sciences · 2017Review
- Natural Compounds As Modulators of Non-apoptotic Cell Death in Cancer Cells.Current genomics · 2017Article
- Tumor Protein (TP)-p53 Members as Regulators of Autophagy in Tumor Cells upon Marine Drug Exposure.Marine drugs · 2016Article
- The microRNA feedback regulation of p63 in cancer progression.Oncotarget · 2015Review
- Phospho-ΔNp63α/microRNA network modulates epigenetic regulatory enzymes in squamous cell carcinomas.Cell cycle (Georgetown, Tex.) · 2014Article
- Phospho-ΔNp63α/microRNA feedback regulation in squamous carcinoma cells upon cisplatin exposure.Cell cycle (Georgetown, Tex.) · 2013Article
- p63 the guardian of human reproduction.Cell cycle (Georgetown, Tex.) · 2012Review
- Advances in targeting signal transduction pathways.Oncotarget · 2012Review
- Tissue-specific expression of p73 C-terminal isoforms in mice.Cell cycle (Georgetown, Tex.) · 2012Article
- Article
- Recent progress in genetics of aging, senescence and longevity: focusing on cancer-related genes.Oncotarget · 2012Review
- Phospho-ΔNp63α/SREBF1 protein interactions: bridging cell metabolism and cisplatin chemoresistance.Cell cycle (Georgetown, Tex.) · 2012Article
- Phospho-ΔNp63α-dependent regulation of autophagic signaling through transcription and micro-RNA modulation.Cell cycle (Georgetown, Tex.) · 2012Article
- Tumor protein p63/nuclear factor κB feedback loop in regulation of cell death.The Journal of biological chemistry · 2011Article
- Recent progress in targeting cancer.Aging · 2011Review
- Phospho-ΔNp63α/miR-885-3p axis in tumor cell life and cell death upon cisplatin exposure.Cell cycle (Georgetown, Tex.) · 2011Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress was shown to promote the translocation of Ataxia-telangiectasia mutated (ATM) to cytoplasm and trigger the LKB1-AMPK-tuberin pathway leading to a down-regulation of mTOR and subsequently inducing the programmed cell death II (autophagy). Cisplatin was previously found to induce the ATM-dependent phosphorylation of ΔNp63α in squamous cell carcinoma (SCC) cells. In this study, phosphorylated (p)-ΔNp63α was shown to bind the ATM promoter, to increase the ATM promoter activity and to enhance the ATM cytoplasmic accumulation. P-ΔNp63α protein was further shown to interact with the Rpn13 protein leading to a proteasome-dependent degradation of p-ΔNp63α and thereby protecting LKB1 from the degradation. In SCC cells (with an altered ability to support the ATM-dependent ΔNp63α phosphorylation), the non-phosphorylated ΔNp63α protein failed to form protein complexes with the Rpn13 protein and thereby allowing the latter to bind and target LKB1 into a proteasome-dependent degradation pathway thereby modulating a cisplatin-induced autophagy. We thus suggest that SCC cells sensitive to cisplatin-induced cell death are likely to display a greater ratio of p-ΔNp63α/non-phosphorylated ΔNp63α than cells with the innate resistant/impaired response to a cisplatin-induced cell death. Our data also suggest that the choice made by Rpn13 between p-ΔNp63α or LKB1 to be targeted for degradation is critical for cell death decision made by cancer cells in response to chemotherapy.
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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.