ArticleAging2015
The p53 tumor suppressor protein protects against chemotherapeutic stress and apoptosis in human medulloblastoma cells.
Article in Aging, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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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
14 citing papers in PubMed, 23 citations in OpenAlex.
- Revolutionizing cancer care strategies: immunotherapy, gene therapy, and molecular targeted therapy.Molecular biology reports · 2024Review
- Modulation of Viability, Proliferation, and Stemness by Rosmarinic Acid in Medulloblastoma Cells: Involvement of HDACs and EGFR.Neuromolecular medicine · 2023Article
- MDM2- an indispensable player in tumorigenesis.Molecular biology reports · 2023Review
- Expansion of human amniotic epithelial cells using condition cell reprogramming technology.Human cell · 2023Article
- An immune infiltration-related prognostic model of kidney renal clear cell carcinoma with two valuable markers: CAPN12 and MSC.Frontiers in oncology · 2023Article
- Regulation of Chemosensitivity in Human Medulloblastoma Cells by p53 and the PI3 Kinase Signaling Pathway.Molecular cancer research : MCR · 2022Article
- Per- and polyfluoroalkyl substances, epigenetic age and DNA methylation: a cross-sectional study of firefighters.Epigenomics · 2021Article
- The Effects of P53 in the Globular Heads of the C1q Receptor in Gastric Carcinoma Cell Apoptosis Are Exerted via a Mitochondrial-Dependent Pathway.Doklady. Biochemistry and biophysics · 2021Article
- Specific Protein 1 and p53 Interplay Modulates the Expression of the KCTD-Containing Cullin3 Adaptor Suppressor of Hedgehog 2.Frontiers in cell and developmental biology · 2021Article
- Chemical modulation of autophagy as an adjunct to chemotherapy in childhood and adolescent brain tumors.Oncotarget · 2018Review
- Article
- Significance of Wild-Type p53 Signaling in Suppressing Apoptosis in Response to Chemical Genotoxic Agents: Impact on Chemotherapy Outcome.International journal of molecular sciences · 2017Review
- Zinc and zinc-containing biomolecules in childhood brain tumors.Journal of molecular medicine (Berlin, Germany) · 2016Review
- The Growing Complexity of Cancer Cell Response to DNA-Damaging Agents: Caspase 3 Mediates Cell Death or Survival?International journal of molecular sciences · 2016Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
Abstract
Medulloblastoma (MB), a primitive neuroectodermal tumor, is the most common malignant childhood brain tumor and remains incurable in about a third of patients. Currently, survivors carry a significant burden of late treatment effects. The p53 tumor suppressor protein plays a crucial role in influencing cell survival in response to cellular stress and while the p53 pathway is considered a key determinant of anti-tumor responses in many tumors, its role in cell survival in MB is much less well defined. Herein, we report that the experimental drug VMY-1-103 acts through induction of a partial DNA damage-like response as well induction of non-survival autophagy. Surprisingly, the genetic or chemical silencing of p53 significantly enhanced the cytotoxic effects of both VMY and the DNA damaging drug, doxorubicin. The inhibition of p53 in the presence of VMY revealed increased late stage apoptosis, increased DNA fragmentation and increased expression of genes involved in apoptosis, including CAPN12 and TRPM8, p63, p73, BIK, EndoG, CIDEB, P27Kip1 and P21cip1. These data provide the groundwork for additional studies on VMY as a therapeutic drug and support further investigations into the intriguing possibility that targeting p53 function may be an effective means of enhancing clinical outcomes in MB.
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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.