We are analyzing https://link.springer.com/article/10.1007/s10495-007-0082-8.

Title:
Apoptosis by cisplatin requires p53 mediated p38α MAPK activation through ROS generation | Apoptosis
Description:
Cisplatin is one of the major chemotherapeutic weapons used against different human cancers, although its mechanism to induce apoptosis is not fully understood. The presence of wild type p53 has been suggested to be important for cisplatin cytotoxicity, hence we found that cisplatin induced apoptosis in cell lines with functional p53. Using the HCT116 colon carcinoma derived cell line we have established that the apoptotic activity of cisplatin requires the onset of a p53-mediated p38α MAPK pathway through generation of reactive oxygen species (ROS). HCT116 p53-deficient cells were much less sensitive to apoptosis by cisplatin than their p53wt counterparts, where apoptosis was strongly inhibited by antioxidants. Moreover, the presence of pifithrin-α, an inhibitor of p53 transcriptional activity, blocked cisplatin-induced apoptosis, reduced the generation of ROS produced upon cisplatin treatment. In addition, we have identified p38α as the isoform necessary for cisplatin-induced apoptosis, upon activation by p53-mediated ROS production. p38α MAPK contributes to further activation of p53, which leads to a positive feedback loop, p38α MAPK/p53. We conclude that the p53/ROS/p38α MAPK cascade is essential for cisplatin-induced cell death in HCT116 cells and the subsequent p38α/p53 positive feedback loop strongly enhances the initial p53 activation.
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Keywords {🔍}

article, pubmed, google, scholar, cas, apoptosis, activation, cell, cisplatin, biol, role, kinase, mapk, ros, protein, phosphorylation, pathway, access, cancer, porras, human, cells, transcriptional, cisplatininduced, death, chem, privacy, essential, cookies, content, almudena, reactive, oxygen, information, publish, search, generation, bragado, silva, activity, species, signaling, open, dna, res, regulation, oncogene, kang, author, data,

Topics {✒️}

p53/ros/p38α mapk cascade transcription-independent pro-apoptotic functions cisplatin-induced cell death p38/atf-7 signaling pathway p38 mapk/mk2 pathway p38 mapk-mediated activation atr-mediated checkpoint signaling month download article/chapter doxorubicin-induced dna intercalation activated p38 mapk transcription-independent apoptosis triggered positive feedback loop blocked cisplatin-induced apoptosis sanchez-arevalo lobo vj p53-mediated ros production cell death induced bpde-induced p53 accumulation p38 mapk pathway p53-deficient cells rely hct116 p53-deficient cells p38 map kinase cellular components involved p38α mapk/p53 almudena porras p38α mapk contributes machine learning related subjects article apoptosis aims full article pdf cisplatin induced apoptosis cisplatin-induced apoptosis p38alpha map kinase reactive oxygen species dna damage author information authors privacy choices/manage cookies p53-dependent apoptosis uvb-mediated activation uncoupling protein expression p53 tumor suppressor hct116-p53-deficient enhanced ros production p38 mapk cisplatin based therapy cisplatin-based therapy human melanoma cells article bragado facultad de farmacia cisplatin requires check access

Questions {❓}

Slee EA, O’Connor DJ, Lu X (2004) To die or not to die: how does p53 decide?

Schema {🗺️}

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         description:Cisplatin is one of the major chemotherapeutic weapons used against different human cancers, although its mechanism to induce apoptosis is not fully understood. The presence of wild type p53 has been suggested to be important for cisplatin cytotoxicity, hence we found that cisplatin induced apoptosis in cell lines with functional p53. Using the HCT116 colon carcinoma derived cell line we have established that the apoptotic activity of cisplatin requires the onset of a p53-mediated p38α MAPK pathway through generation of reactive oxygen species (ROS). HCT116 p53-deficient cells were much less sensitive to apoptosis by cisplatin than their p53wt counterparts, where apoptosis was strongly inhibited by antioxidants. Moreover, the presence of pifithrin-α, an inhibitor of p53 transcriptional activity, blocked cisplatin-induced apoptosis, reduced the generation of ROS produced upon cisplatin treatment. In addition, we have identified p38α as the isoform necessary for cisplatin-induced apoptosis, upon activation by p53-mediated ROS production. p38α MAPK contributes to further activation of p53, which leads to a positive feedback loop, p38α MAPK/p53. We conclude that the p53/ROS/p38α MAPK cascade is essential for cisplatin-induced cell death in HCT116 cells and the subsequent p38α/p53 positive feedback loop strongly enhances the initial p53 activation.
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      headline:Apoptosis by cisplatin requires p53 mediated p38α MAPK activation through ROS generation
      description:Cisplatin is one of the major chemotherapeutic weapons used against different human cancers, although its mechanism to induce apoptosis is not fully understood. The presence of wild type p53 has been suggested to be important for cisplatin cytotoxicity, hence we found that cisplatin induced apoptosis in cell lines with functional p53. Using the HCT116 colon carcinoma derived cell line we have established that the apoptotic activity of cisplatin requires the onset of a p53-mediated p38α MAPK pathway through generation of reactive oxygen species (ROS). HCT116 p53-deficient cells were much less sensitive to apoptosis by cisplatin than their p53wt counterparts, where apoptosis was strongly inhibited by antioxidants. Moreover, the presence of pifithrin-α, an inhibitor of p53 transcriptional activity, blocked cisplatin-induced apoptosis, reduced the generation of ROS produced upon cisplatin treatment. In addition, we have identified p38α as the isoform necessary for cisplatin-induced apoptosis, upon activation by p53-mediated ROS production. p38α MAPK contributes to further activation of p53, which leads to a positive feedback loop, p38α MAPK/p53. We conclude that the p53/ROS/p38α MAPK cascade is essential for cisplatin-induced cell death in HCT116 cells and the subsequent p38α/p53 positive feedback loop strongly enhances the initial p53 activation.
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