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Potential Role of TRAIL in Metastasis of Mutant KRAS Expressing Lung Adenocarcinoma | Cancer Microenvironment
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Apo2L/tumor necrosis factor (TNF)-α-related apoptosis-inducing ligand (TRAIL, TNFSF10) is an important cytokine in the tumor microenvironment and plays a major role in the balance of cell survival/death pathways. Bioinformatic analyses of 839 adenocarcinoma (AC) and 356 squamous cell lung carcinoma patient data (SCC) by cBioPortal (genomic analyses) shows that TRAIL expression leads to differential outcomes of disease free survival in AC and SCC. Oncomine datamining (transcript analyses) reveal that TRAIL is upregulated in 167 SCC as compared to 350 AC patients from six data sets. Genomic analyses using cBioPortal revealed high rates of KRAS mutation in AC accompanied by higher incidence of metastasis and increased amplifications of TRAIL gene in SCC. Bioinformatic analyses of an additional lung cancer patient database also showed that risk of disease progression was significantly increased with high TRAIL expression in AC (461 samples). In vitro studies demonstrated that TRAIL increased phosphorylation of ERK only in adenocarcinoma cell lines with mutant KRAS. This was associated with increased migration that was abrogated by MEK inhibitor PD98059. Effects of increased migration induced by TRAIL persisted even after exposure to ionizing radiation with suppression of DNA damage response. These results help understand the role of TRAIL signaling in metastasis which is essential to develop strategies to revert these signals into pro-apoptotic pathways.
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cancer, pubmed, article, google, scholar, trail, cas, lung, cell, central, death, data, metastasis, kras, adenocarcinoma, expression, cells, privacy, cookies, research, analyses, increased, signaling, resistance, nonsmall, apoptosis, content, information, publish, search, microenvironment, role, mutant, pal, amin, scc, access, res, trailinduced, human, analysis, log, journal, track, april, shyama, prayag, sainis, bhavani, shankar,
Topics {✒️}
α-related apoptosis-inducing ligand ifn-gamma-enhanced trail-induced apoptosis death receptor–induced apoptosis tumor-cell resistance small-cell lung cancer month download article/chapter cancer cell-autonomous trail death ligand trail cell survival/death pathways canonical kinase signaling dna damage response trail-induced iap-2 upregulation lung cancer cells integrated data-mining platform death receptor family trail-induced apoptosis adenocarcinoma cell lines mutant kras contributing factor full article pdf trail resistance squamous cell prognosis-related genes cancer microarray database tumor microenvironment ifn-gamma inhibition trail death receptors privacy choices/manage cookies trail promotes metastasis induces apoptosis von karstedt quantifying cell phenotypes clin cancer res dna methylation levels high trail expression lung cancer trail signaling metastasis-promoting receptors trail expression leads article pal cancer cell 27 pro-apoptotic pathways image analysis software cancer cells related subjects cancer microenvironment 9 disease free survival european economic area vitro studies demonstrated main histologic types
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headline:Potential Role of TRAIL in Metastasis of Mutant KRAS Expressing Lung Adenocarcinoma
description:Apo2L/tumor necrosis factor (TNF)-α-related apoptosis-inducing ligand (TRAIL, TNFSF10) is an important cytokine in the tumor microenvironment and plays a major role in the balance of cell survival/death pathways. Bioinformatic analyses of 839 adenocarcinoma (AC) and 356 squamous cell lung carcinoma patient data (SCC) by cBioPortal (genomic analyses) shows that TRAIL expression leads to differential outcomes of disease free survival in AC and SCC. Oncomine datamining (transcript analyses) reveal that TRAIL is upregulated in 167 SCC as compared to 350 AC patients from six data sets. Genomic analyses using cBioPortal revealed high rates of KRAS mutation in AC accompanied by higher incidence of metastasis and increased amplifications of TRAIL gene in SCC. Bioinformatic analyses of an additional lung cancer patient database also showed that risk of disease progression was significantly increased with high TRAIL expression in AC (461 samples). In vitro studies demonstrated that TRAIL increased phosphorylation of ERK only in adenocarcinoma cell lines with mutant KRAS. This was associated with increased migration that was abrogated by MEK inhibitor PD98059. Effects of increased migration induced by TRAIL persisted even after exposure to ionizing radiation with suppression of DNA damage response. These results help understand the role of TRAIL signaling in metastasis which is essential to develop strategies to revert these signals into pro-apoptotic pathways.
datePublished:2016-04-23T00:00:00Z
dateModified:2016-04-23T00:00:00Z
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TRAIL
cBioPortal
Oncomine
Adenocarcinoma
Squamous cell carcinoma
Mutant KRAS
ERK signaling
Cancer Research
Oncology
Immunology
Cell Biology
Biochemistry
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Biomedicine
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headline:Potential Role of TRAIL in Metastasis of Mutant KRAS Expressing Lung Adenocarcinoma
description:Apo2L/tumor necrosis factor (TNF)-α-related apoptosis-inducing ligand (TRAIL, TNFSF10) is an important cytokine in the tumor microenvironment and plays a major role in the balance of cell survival/death pathways. Bioinformatic analyses of 839 adenocarcinoma (AC) and 356 squamous cell lung carcinoma patient data (SCC) by cBioPortal (genomic analyses) shows that TRAIL expression leads to differential outcomes of disease free survival in AC and SCC. Oncomine datamining (transcript analyses) reveal that TRAIL is upregulated in 167 SCC as compared to 350 AC patients from six data sets. Genomic analyses using cBioPortal revealed high rates of KRAS mutation in AC accompanied by higher incidence of metastasis and increased amplifications of TRAIL gene in SCC. Bioinformatic analyses of an additional lung cancer patient database also showed that risk of disease progression was significantly increased with high TRAIL expression in AC (461 samples). In vitro studies demonstrated that TRAIL increased phosphorylation of ERK only in adenocarcinoma cell lines with mutant KRAS. This was associated with increased migration that was abrogated by MEK inhibitor PD98059. Effects of increased migration induced by TRAIL persisted even after exposure to ionizing radiation with suppression of DNA damage response. These results help understand the role of TRAIL signaling in metastasis which is essential to develop strategies to revert these signals into pro-apoptotic pathways.
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TRAIL
cBioPortal
Oncomine
Adenocarcinoma
Squamous cell carcinoma
Mutant KRAS
ERK signaling
Cancer Research
Oncology
Immunology
Cell Biology
Biochemistry
general
Biomedicine
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