ArticleNeoplasia (New York, N.Y.)2008
Cyclic pifithrin-alpha sensitizes wild type p53 tumor cells to antimicrotubule agent-induced apoptosis.
Article in Neoplasia (New York, N.Y.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
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Who cites it
15 citing papers in PubMed, 30 citations in OpenAlex.
- Anti-invasive effects of CXCR4 and FAK inhibitors in non-small cell lung carcinomas with mutually inactivated p53 and PTEN tumor suppressors.Investigational new drugs · 2017Article
- Do Multiwell Plate High Throughput Assays Measure Loss of Cell Viability Following Exposure to Genotoxic Agents?International journal of molecular sciences · 2017Article
- 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
- Transcriptional and Post-Transcriptional Regulation of Thrombospondin-1 Expression: A Computational Model.PLoS computational biology · 2017Article
- The Growing Complexity of Cancer Cell Response to DNA-Damaging Agents: Caspase 3 Mediates Cell Death or Survival?International journal of molecular sciences · 2016Review
- Modulation of the pentose phosphate pathway alters phase I metabolism of testosterone and dextromethorphan in HepG2 cells.Acta pharmacologica Sinica · 2015Article
- Cisplatin-induced renal injury is independently mediated by OCT2 and p53.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Article
- Contractile forces sustain and polarize hematopoiesis from stem and progenitor cells.Cell stem cell · 2014Article
- Pseudolaric Acid B induces caspase-dependent and caspase-independent apoptosis in u87 glioblastoma cells.Evidence-based complementary and alternative medicine : eCAM · 2012Article
- Article
- RETRACTED: Synergistic antitumor effects of novel HDAC inhibitors and paclitaxel in vitro and in vivo.PloS one · 2011Article
- Dinosaurs and ancient civilizations: reflections on the treatment of cancer.Neoplasia (New York, N.Y.) · 2010Article
- Hypoxia downregulates p53 but induces apoptosis and enhances expression of BAD in cultures of human syncytiotrophoblasts.American journal of physiology. Cell physiology · 2010Article
- The War on Cancer rages on.Neoplasia (New York, N.Y.) · 2009Article
- Neoplasia: the second decade.Neoplasia (New York, N.Y.) · 2008Article
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
As a consequence of multiple functions of p53, its activation in response to cytotoxic stress may have proapoptotic or protective effects depending on the nature of lesions. We have previously shown that mutational inactivation of p53 results in sensitization to paclitaxel. In this study, we used cyclic pifithrin-alpha, a transcriptional inhibitor of p53, to further investigate the relevance of p53 function in the response of tumor cells to microtubule inhibitors. Using drug concentrations causing only antiproliferative effects, the combination of antimicrotubule agents with subtoxic pifithrin-alpha doses resulted in increase of sensitivity of two wild type p53 cell lines, associated with a substantial M phase cell accumulation and marked sensitization to apoptosis. Pifithrin-alpha had no sensitizing effect in p53 defective cells or a marginal effect in normal human fibroblasts. The apoptotic response to the combination was concomitant with p21 down-regulation, Polo-like kinase 1 up-regulation, p34(cdc2) kinase dephosphorylation, and cdc25C phosphatase phosphorylation, supporting mitotic arrest. Sensitization to paclitaxel-induced apoptosis was also achieved by p53-siRNA transfection in wild type p53 H460 cells. Pifithrin-alpha did not enhance the apoptotic response after p53 down-regulation. The results support a protective role of the transcriptional activity of p53 in response to mitotic spindle damage. The inhibition of transcriptional activity of p53 may have therapeutic implications in the treatment of p53 wild type tumors with antimitotic agents.
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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.