Project description:OCC-1 is one of the earliest annotated long noncoding RNAs (lncRNAs) in colorectal cancer (CRC). In our study, we found that knockdown of OCC-1 by shRNAs promotes CRC cell growth both in vitro and in vivo. To gain insight into the molecular function of OCC-1, we profiled the gene expression of Caco-2 cells after OCC-1 knockdown by microarray.
Project description:BORIS expresses abnormally in colorectal cancer cells. Both the expression and the copy number of BORIS are remarkably higher in colorectal cancer cells than in normal colon or rectal cells. BORIS is potential diagnosis, prognosis or therapeutic target for colorectal cancer. To expand our view of the signaling pathway related with BORIS, altered gene expression by BORIS knockdown was assessed by microarray assay. To study the gene regulation by BORIS knockdown, microarray assay was applied to screen the gene expression regulated by BORIS siRNA in colorectal cancer cells HCT116 and Caco-2
Project description:LC-MS/MS glycoproteomic analysis of EGFR N-glycosylation profile. EGFR immunoprecipitated from colorectal cancer cell lines SW48 (wild-type and ST6Gal1 overexpression) and Caco-2 (wild-type and ST6Gal1 knock-out)
Project description:MicroRNAs regulate the biological aggressiveness of colorectal cancer (CRC) cells and might serve as potential prognostic factors and therapeutic targets. In this study, we therefore globally profiled microRNAs associated with aggressive growth in CRC cells, in an attempt to identify novel prognostic biomarkers in CRC patients. In detail, two different CRC cell lines (Caco-2 and HRT-18) with completely different growth rates and different E-cadherin expression were profiled for differences in more than 1000 human microRNAs by using microarray technology. Two-condition experiment, HRT-18 vs. Caco-2. Biological replicates: 3, independently grown and harvested. On each array, one BR of HRT-18 cells was directly compared to one BR of Caco-2 cells (serving as reference sample). All hybridizations were repeated with reversed dye assignment (dye-swap) as technical replicates.
Project description:MicroRNAs regulate the biological aggressiveness of colorectal cancer (CRC) cells and might serve as potential prognostic factors and therapeutic targets. In this study, we therefore globally profiled microRNAs associated with aggressive growth in CRC cells, in an attempt to identify novel prognostic biomarkers in CRC patients. In detail, two different CRC cell lines (Caco-2 and HRT-18) with completely different growth rates and different E-cadherin expression were profiled for differences in more than 1000 human microRNAs by using microarray technology.
Project description:Lipid metabolism reprogramming is a well-established hallmark of many cancer types, including colorectal cancer (CRC). Nevertheless, a clear understanding on how fatty acid (FA) metabolism is fine-tuned during CRC development and progression is still missing. Given that CRC is the second leading cause of cancer-related death, addressing these critical aspects may provide the rationale for new therapeutic approaches and early biomarker identification. Fatty acid binding protein 1 (FABP1) is a small protein that binds FA and other lipophilic compounds, acting as a lipid transporter in the intestine. Little is currently known about the function of FABP1 in CRC. Here we show that the knockdown of FABP1 in CRC cells impairs de novo FA and cholesterol synthesis, specifically, via altering the transcriptional regulation of lipid metabolism genes. FABP1 depletion suppresses the expression of FA and cholesterol synthesis-associated genes while promoting that of FA oxidation genes and mitochondrial oxidative pathways. The latter is associated with increased oxygen consumption rate and activation of the energy sensor 5’ AMP-activated kinase (AMPK). Taken together, our results show that FABP1 orchestrates the balance between FA synthesis and oxidation, most likely to prevent the cytotoxic effects of circulating unbound free fatty acids. Thus, targeting FABP1 function may represent a potential therapeutic strategy in advanced CRC
Project description:Interferon-induced transmembrane protein 1 (IFITM1) is one of the three members of the interferon-induced transmembrane family and has recently been identified as a new molecular marker in human colorectal cancer. However, its functional roles in colorectal cancer are still elusive. In this study, we investigate the gene expression profiling of HT-29 cells with IFITM1 knockdown. We revealed that several invasive- and carcinogenesis-related genes were differentially expressed. We transfected siRNAs targeting firefly luciferase and human IFITM1 mRNAs into HT-29 colorectal adenocarcinoma cells. At 72 h post-transfection, total RNA was harvested for microarray hybridization. A siLuc-transfected sample was used as the baseline control.