The tumor microenvironment is characterized by low glucose and hypoxia. It is well known that changes in the tumor microenvironment, such as hypoxia and low glucose, can increase the production of VEGF. Although the role of hypoxia in the regulation of VEGF production is well understood, the mechanism linking glucose deprivation (GD) to tumor growth and angiogenesis is unclear. Here, GD (a physiological stimulus) was used to treat human tumor cells. The transcriptional reprogramming of tumor cells by GD was measured with microarray technology to provide a comprehensive analysis of the gene expression profile underlying the GD treatment. Our study suggested that GD initiates an angiogenic switch by increasing the expression of proangiogenic mediators (VEGF, FGF2, IL6, etc.) and decreasing the expression of angiogenesis inhibitors (THBS1, CXCL14 and CXCL10). The markers of Unfolded Protein Response (UPR) (Grp78/Bip, CHOP, ATF4, etc.) were significantly increased. The above results suggest GD may regulate angiogenesis through activation of the UPR.
The unfolded protein response induces the angiogenic switch in human tumor cells through the PERK/ATF4 pathway.
Specimen part, Cell line, Treatment
View SamplesThe majority of cancer patients do not respond to immunotherapy. In order to systematically discover pathways promoting cancer cell resistance to effector immune cells, we generated immunity-resistant Head and Neck Squamous Cell Carcinoma cell lines. We utilized RNA-Seq to determine what are the genes and pathways that are significantly altered when cancer cells become resistant to effectors. Overall design: RNA-Seq was performed on four cell lines, including two biologic replicates of wildtype and immune-resistant PCI-13 cells. The two immune-resistant PCI-13 cell lines were generated separately using the same protocol described in the manuscript.
Mitigating SOX2-potentiated Immune Escape of Head and Neck Squamous Cell Carcinoma with a STING-inducing Nanosatellite Vaccine.
Sex, Specimen part, Cell line, Subject
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