Project description:KYSE410 cells were tranfected with NOX5 plasmid in the presence or absence of HIF-1α inhibitor-BAY87-2243 and mRNA expression of tumor-promoting molecules were assayed by RiboArray Human mRNA Array investigation of the critical gene participating in the process of NOX5/HIF-1α-mediated ESCC progression.
Project description:Primary outcome(s): Relationship with mRNA expression of B7 family molecules in blood of patients with colorectal cancer and clinicopathological factors
Project description:Cancer-associated fibroblasts (CAFs), the principal components of tumor microenvironment, play multiple roles in breast cancer onset and progression. While their impact is widely accepted, treatment options to target CAFs in clinical practice were not yet well established. The nuclear receptor superfamily encompasses a druggable class of molecules, expressed in various stroma and parenchymal cell types, with the interesting therapeutic potential to modulate the reactive microenvironment. Having already addressed the oncosuppressive role of the nuclear Farnesoid X Receptor (FXR) in mammary epithelial cancer cells, the present study is aimed to assess the function of FXR in CAFs and evaluate whether its activation may affect their tumor-promoting features.
Project description:KYSE410 cells were treated with PBS, TNFα, IL1β, and LPS respectively and mRNA expression profiles were assayed by Nimblegen gene expression microarray human HG18 (12x135K) Investigation of the critical gene participating various inflammatory stimuli in the process of ESCC progression.
Project description:In this study we obtained gene expression profiles of MCFS and parental MCF7 cell lines using Illumina microarrays Transcriptome analysis of tumor promoting mammospheres (MCFS) and parental MCF7 breast cancer cell line was run in triplicate on microarrays
Project description:VEGF165 is one of the key regulators of tumor development. Using HCT116 cells transfected with full-length vegf mRNA, full-length vegf mRNA with mutations of H9D and L14E, mutated vegf mRNAs lacking untranslated regions (UTRs), and 5’UTR mutated between nt 591 and nt 746, we found that vegf 5’UTR resided an anti-apoptotic activity against chemotherapy independently of VEGF165. We next established HCT116 clones stably expressing vegf 5’UTR or the mutated vegf 5’UTR. The cells expressing 5’UTR, but not the mutated UTR, showed the drug-resistant phenotype, anchorage-independent growth, and rapid tumor growth when implanted in athymic nude mice. Microarray and real-time PCR showed that the vegf 5’UTR-expressing tumors up-regulated anti-apoptotic genes including mia and down-regulated pro-apoptotic genes including fas, pdcd1, nrg1, and bax. Microarray analysis also revealed specific down-regulation of IFN-inducible genes (43 genes) in the growing tumors. HCT116 cells stably transcribing vegf 5’UTR decreased STAT1 expression and IFN alpha-STAT1 pathway. In addition to 5-fluorouracil treatment, the vegf 5’UTR-expressing tumors did not respond to IFN alpha therapy at all. This novel tumor-promoting function in the vegf 5’UTR may partly explain the insufficiency of the VEGF-VEGFR strategies and suggest a vegf-targeted silencing strategy as a more effective anti-tumor therapy. Keywords: genetic modification