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Expression data from SW1990, HCT-116 and Hep3B cancer cell lines

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE99213 | GEO | 2017/05/23

SECONDARY ACCESSION(S): PRJNA387575

REPOSITORIES: GEO

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Expression data from SW1990, HCT-116 and Hep3B cancer cell lines

Project description:Expression data from SW1990, HCT-116 and Hep3B cancer cell lines

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Cytotoxic and apoptotic potential of gemini-chrysophanol nanoparticles against human colorectal cancer HCT-116 cell lines.

Project description:BackgroundColorectal cancer is among the most common cancers and accounts for nearly 9% of all cancers in the world. Chrysophanol is a naturally occurring anthraquinone exerts a number of pharmacological activities such as anti-inflammation, anti-cancer, anti-bacterial, anti-viral, and anti-oxidant effects. This study aims to produce a novel gemini chrysophanol nanoparticles (Gemini-Chr NPs), and to evaluate its anti-cancer effect on the human colorectal cancer cell lines.MethodsGemini-Chr NPs were synthesized through nanoprecipitation method and characterized by dynamic light scattering and scanning electron microscopy, Anti-cancer activities were examined through MTT assay on HCT-116 cancer cells, apoptosis was investigated via Annexin V-FITC/PI dual stain assay. Furthermore, the expression of Bax, Bcl-2 and P53 genes were evaluated using real-time PCR and western blotting assay. RESULTS: The average particle diameter of the synthesized Gemini-Chr NPs and zeta potential were recorded as 120 nm and 14.4 mV, respectively. In comparison to the normal cells, the cytotoxicity assay confirmed that Gemini-Chr NPs preferentially killed colorectal cancer cells via induction of apoptosis. Moreover, Gemini-Chr NPs could upregulate the expression of Bax in both cancerous and normal cells (p ≤ 0.05) and decreasing the Bcl-2 expression in only tumor cells (p ≤ 0.01), while the expression of P53 is modulated in tumor cells (p ≤ 0.05).ConclusionsGemini surfactants could be considered for efficient delivery and improvement of anti-cancer effect of chrysophanol. Gemini-Chr NPs might have the potential for developing novel therapeutic agent against colorectal cancer.

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Transcriptomic data of bevacizumab-adapted colorectal adenocarcinoma cells HCT-116.

Project description:A bioinformatic approach was applied to evaluate the effect of treatment with Bevacizumab on the gene expression profile of colorectal adenocarcinoma cells. The transcriptomic profile of Bevacizumab-adapted HCT-116 (Bev/A) colorectal adenocarcinoma cells was determined and compared with that of the corresponding control cell line by Agilent microarray analysis. Raw data were preprocessed, normalized, filtered, and subjected to a differential expression analysis using standard R/Bioconductor packages (i.e., limma, RankProd). As consequence of Bevacizumab adaptation, 166 differentially expressed genes (DEGs) emerged, most of them (123) resulted downregulated and 43 overexpressed. The list of statistically significant dysregulated genes was used as an input for functional overrepresentation analysis using ToppFun web tool. Such analysis pointed at cell adhesion, cell migration, extracellular matrix organization and angiogenesis as the main dysregulated biological process involved in Bevacizumab-adaptation of HCT116 cells. In addition, gene set enrichment analysis was performed using GSEA, searching for enriched terms within the Hallmarks (H), Canonical Pathways (CP), and Gene Ontology (GO) gene sets. GO terms that showed significant enrichment included: transportome, vascularization, cell adhesion and cytoskeleton, extra cellular matrix (ECM), differentiation and epithelial-mesenchymal transition (EMT), inflammation and immune response. Raw and normalized microarray data were deposited in the Gene Expression Omnibus (GEO) public repository with accession number GSE221948.

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Expression data from colorectal cancer cell line HCT-116

Project description:We used microarrays to detail the global gene expression in cell line with or without M1 virus infection.

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MicroRNA profiling of HCT-116 versus HCT-116 treated with 5-aza-2'-deoxycytidine processing human colon cancer cell lines

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Expression data in HCT-116 colon cancer cell treated with SCD1 inhibitor or in SCD1 knocked out HCT-116 cell

Project description:To understand molecular mechanisms underlying the growth inhibitory ativity of Stearoyl-CoA desaturase-1 (SCD1) inhibitor, we performed microarray analysis using HCT-116 colorectal cancer cells, in which SCD1 was pharmacologically blocked or genetically ablated.

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Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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Radiation-Induced Senescence Reprograms Secretory and Metabolic Pathways in Colon Cancer HCT-116 Cells.

Project description:Understanding the global metabolic changes during the senescence of tumor cells can have implications for developing effective anti-cancer treatment strategies. Ionizing radiation (IR) was used to induce senescence in a human colon cancer cell line HCT-116 to examine secretome and metabolome profiles. Control proliferating and senescent cancer cells (SCC) exhibited distinct morphological differences and expression of senescent markers. Enhanced secretion of pro-inflammatory chemokines and IL-1, anti-inflammatory IL-27, and TGF-β1 was observed in SCC. Significantly reduced levels of VEGF-A indicated anti-angiogenic activities of SCC. Elevated levels of tissue inhibitors of matrix metalloproteinases from SCC support the maintenance of the extracellular matrix. Adenylate and guanylate energy charge levels and redox components NAD and NADP and glutathione were maintained at near optimal levels indicating the viability of SCC. Significant accumulation of pyruvate, lactate, and suppression of the TCA cycle in SCC indicated aerobic glycolysis as the predominant energy source for SCC. Levels of several key amino acids decreased significantly, suggesting augmented utilization for protein synthesis and for use as intermediates for energy metabolism in SCC. These observations may provide a better understanding of cellular senescence basic mechanisms in tumor tissues and provide opportunities to improve cancer treatment.

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