We are analyzing https://link.springer.com/article/10.1007/s10495-015-1141-1.

Title:
Inflammation-induced radioresistance is mediated by ROS-dependent inactivation of protein phosphatase 1 in non-small cell lung cancer cells | Apoptosis
Description:
Inflammation plays a pivotal role in modulating the radiation responsiveness of tumors. We determined that an inflammation response prior to irradiation contributes to radiotherapy resistance in non-small cell lung cancer (NSCLC) cells. In the clonogenic survival assay, activation of the inflammation response by lipopolysaccharide (LPS) decreased the degree of radiosensitivity in NCI-H460 cells (relatively radiosensitive cells), but had no effect in A549 cells (relatively radioresistant cells). LPS-induced radioresistance of NCI-H460 cells was also confirmed with a xenograft mouse model. The radioresistant effect observed in NCI-H460 cells was correlated with inhibition of apoptotic cell death due to reduced Caspase 3/7 activity. Moreover, we found that the levels of reactive oxygen species (ROS) were synergistically elevated in NCI-H460 cells by treatment with LPS and radiation. Increased ROS generation negatively affected the activity of protein phosphatase 1 (PP1). Decreased PP1 activity did not lead to Bad dephosphorylation, consequently resulting in the inhibition of irradiation-induced mitochondrial membrane potential loss and apoptosis. We confirmed that pre-treatment with a PP1 activator and LPS sensitized NCI-H460 cells to radiation. Taken together, our findings provided evidence that PP1 activity is critical for radiosensitization in NSCLC cells and PP1 activators can serve as promising radiosensitizers to improve therapeutic efficacy.
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Keywords {🔍}

pubmed, article, google, scholar, cancer, cas, cells, cell, lung, youn, kim, protein, central, radiation, radioresistance, nonsmall, apoptosis, inflammation, research, phosphatase, yang, biol, kang, response, activity, res, human, privacy, cookies, content, ncih, oncol, wang, phosphorylation, int, phosphatases, mol, radiationinduced, publish, search, buhyun, nsclc, activation, radiosensitivity, effect, inhibition, reactive, oxygen, species, ros,

Topics {✒️}

erks/dna-pkcs/hif-1alpha functional interplay tnf-alpha/ros/hif-1-induced upregulation hsf1/sesn3/p21cip1/waf1 pathways induce epithelial-mesenchymal transition month download article/chapter inducible nf-kappab activity small-cell lung cancers radiation-induced cell signaling dna-pkcs inhibitor cell type-specific alterations ras-activated bad phosphatase endotoxin-stimulated blood platelets busandaehak-ro 63beon-gil ionizing radiation-induced responses protein ser/thr phosphatases dna damage response reactive oxygen species inflammation-induced radioresistance subsequent akt-mediated phosphorylation induces bad-mediated apoptosis full article pdf protein phosphatase 1alpha induced pulmonary inflammation serine/threonine phosphatases prolonged cell injury article apoptosis aims lps-induced radioresistance human tumor cells lung cancer cells ros-dependent inactivation radiation-induced apoptosis regulates ionizing radiation privacy choices/manage cookies improve therapeutic efficacy kinase domain mutations inflammation response prior washington state university nci-h460 cells clonogenic survival assay eif2 alpha phosphorylation national research foundation stem cell traits pancreatic cancer cells colorectal cancer cells prostate cancer cells related subjects article kim ribosomal protein s3 differentiated pc12 cells gamma-ray radiation

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         description:Inflammation plays a pivotal role in modulating the radiation responsiveness of tumors. We determined that an inflammation response prior to irradiation contributes to radiotherapy resistance in non-small cell lung cancer (NSCLC) cells. In the clonogenic survival assay, activation of the inflammation response by lipopolysaccharide (LPS) decreased the degree of radiosensitivity in NCI-H460 cells (relatively radiosensitive cells), but had no effect in A549 cells (relatively radioresistant cells). LPS-induced radioresistance of NCI-H460 cells was also confirmed with a xenograft mouse model. The radioresistant effect observed in NCI-H460 cells was correlated with inhibition of apoptotic cell death due to reduced Caspase 3/7 activity. Moreover, we found that the levels of reactive oxygen species (ROS) were synergistically elevated in NCI-H460 cells by treatment with LPS and radiation. Increased ROS generation negatively affected the activity of protein phosphatase 1 (PP1). Decreased PP1 activity did not lead to Bad dephosphorylation, consequently resulting in the inhibition of irradiation-induced mitochondrial membrane potential loss and apoptosis. We confirmed that pre-treatment with a PP1 activator and LPS sensitized NCI-H460 cells to radiation. Taken together, our findings provided evidence that PP1 activity is critical for radiosensitization in NSCLC cells and PP1 activators can serve as promising radiosensitizers to improve therapeutic efficacy.
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      headline:Inflammation-induced radioresistance is mediated by ROS-dependent inactivation of protein phosphatase 1 in non-small cell lung cancer cells
      description:Inflammation plays a pivotal role in modulating the radiation responsiveness of tumors. We determined that an inflammation response prior to irradiation contributes to radiotherapy resistance in non-small cell lung cancer (NSCLC) cells. In the clonogenic survival assay, activation of the inflammation response by lipopolysaccharide (LPS) decreased the degree of radiosensitivity in NCI-H460 cells (relatively radiosensitive cells), but had no effect in A549 cells (relatively radioresistant cells). LPS-induced radioresistance of NCI-H460 cells was also confirmed with a xenograft mouse model. The radioresistant effect observed in NCI-H460 cells was correlated with inhibition of apoptotic cell death due to reduced Caspase 3/7 activity. Moreover, we found that the levels of reactive oxygen species (ROS) were synergistically elevated in NCI-H460 cells by treatment with LPS and radiation. Increased ROS generation negatively affected the activity of protein phosphatase 1 (PP1). Decreased PP1 activity did not lead to Bad dephosphorylation, consequently resulting in the inhibition of irradiation-induced mitochondrial membrane potential loss and apoptosis. We confirmed that pre-treatment with a PP1 activator and LPS sensitized NCI-H460 cells to radiation. Taken together, our findings provided evidence that PP1 activity is critical for radiosensitization in NSCLC cells and PP1 activators can serve as promising radiosensitizers to improve therapeutic efficacy.
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         Non-small cell lung cancer
         Cancer Research
         Cell Biology
         Oncology
         Biochemistry
         general
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