Anticancer research · 2020
Genomic Database Analysis for Head and Neck Cancer Prevention Targets: MTOR Signal Transduction Pathway.
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Koenigsberg Cynthia, Ondrey Frank G
Аннотация
BACKGROUND: Type II diabetes agents have anticancer effects on head and neck squamous cell carcinoma (HNSCC). The mechanistic target of rapamycin (MTOR) pathway represents a putative target.
MATERIALS AND METHODS: We interrogated an Affymetrix HNSCC dataset for MTOR-related gene expression.
RESULTS: MTOR expression itself was unchanged, but various related genes demonstrated differential expression. Pathway promoters ras homolog (RHEB), MTOR-associated protein (MLST8), and ribosomal protein S6 kinase B1 (RPS6KB1) were up-regulated. Expression of growth suppressors tuberous sclerosis complex 2 (TSC2), programmed cell death 4 (PDCD4), and BCL2 apoptosis regulator-associated agonist of cell death (BAD) were reduced in HNSCC. Upstream, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA), AKT serine/threonine kinase 1 (AKT1), and phosphatase and tensin homolog (PTEN) were up-regulated in cancer.
CONCLUSION: Several MTOR pathway promoters and tumor suppressors were found to be differentially expressed, favoring MTOR pathway up-regulation in HNSCC. Genomic databases can be interrogated to identify intervention targets and endpoints in HNSCC trials.
MATERIALS AND METHODS: We interrogated an Affymetrix HNSCC dataset for MTOR-related gene expression.
RESULTS: MTOR expression itself was unchanged, but various related genes demonstrated differential expression. Pathway promoters ras homolog (RHEB), MTOR-associated protein (MLST8), and ribosomal protein S6 kinase B1 (RPS6KB1) were up-regulated. Expression of growth suppressors tuberous sclerosis complex 2 (TSC2), programmed cell death 4 (PDCD4), and BCL2 apoptosis regulator-associated agonist of cell death (BAD) were reduced in HNSCC. Upstream, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA), AKT serine/threonine kinase 1 (AKT1), and phosphatase and tensin homolog (PTEN) were up-regulated in cancer.
CONCLUSION: Several MTOR pathway promoters and tumor suppressors were found to be differentially expressed, favoring MTOR pathway up-regulation in HNSCC. Genomic databases can be interrogated to identify intervention targets and endpoints in HNSCC trials.
Предметные рубрики MeSH
Apoptosis Regulatory ProteinsClass I Phosphatidylinositol 3-KinasesDatabases, GeneticGene Expression Regulation, NeoplasticHead and Neck NeoplasmsHumansNeoplasm ProteinsPTEN PhosphohydrolaseProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2RNA-Binding ProteinsRas Homolog Enriched in Brain ProteinRibosomal Protein S6 Kinases, 70-kDaSignal TransductionTOR Serine-Threonine KinasesTuberous Sclerosis Complex 2 Proteinbcl-Associated Death ProteinmTOR Associated Protein, LST8 Homolog