Project description:To determine the transcriptomic differences between CT-26 and Colon 26, we sequenced RNA from these cell lines as well as tumors isolated ex vivo from tumor bearing animals at sizes 100, 400 and 800 mm3
Project description:RAW cells,ABHD5-KD RAW cells or those macrophage-primed CT-26 cells were subjected to microarray assays.Each group contain 3 samples.
Project description:Swimming signficantly attenuates tumor growth of CT-26 cells in vivo, and up-regulated 715 transcripts expression, while down-regulated 629 transcripts, comparing to Control group.
Project description:we provide a novel immune repertoire and RNA-seq joint library construction method (IRJL), we used IRJL protocol to compare the transcriptomic and immune repertoire of CT-26 tumor model and normal mouse spleen. Overall, IRJL offers a greatly simplified, shortcut and cost-effective protocol with RNA-seq and immune repertoire.
Project description:In osteolytic tumor, bone resportion can be occured after bone metastasis. Bone metastasis of colorectal cancer can induce obvious bone destruction. Aberrant activation of osteoclasts and the precursors is responsible for tumor-induced osteolysis. The biological process of osteoclast precursors could be modified by different tumor microenvironment. Microarrays were used to detail the differentially expressed genes or non-coding RNAs between normal osteoclast precursors and osteoclast precursors treated by secreta from CT-26 cells.
Project description:Goal of the experiment: To identify transcriptional patterns across tumors from colorectal cancer murine models and normal mouse colon samples at different developmental stages. Experiment description: Colorectal cancer (CRC) results from multiple genetic and epigenetic events that produce variable histologies and clinical outcomes. To identify gene regulatory programs that underlie colon tumorigenesis, we profiled gene expression in 39 mouse colon tumors from four independent mouse models and compared this to mouse colon embryonic development, as well as with 100 human colon carcinomas. Here, we report a striking recapitulation of embryonic patterns of gene expression in both mouse and human colon tumors. All four of the mouse colon tumor models exhibited large-scale activation of embryonic gene expression signatures. The two nuclear beta-catenin-positive mouse tumors (azoxymethane-treated [AOM] and ApcMin/+), exhibited strong activation of genes characteristic of those expressed in the earliest embryonic stages, while tumors from two other models (Smad3-/- and Tgfb1-/- x Rag2-/-) exhibited lower activation of early stage-specific genes but substantial expression of general embryonic colon genes. Human colon cancer cases over-expressed genes characteristic of both early and late embryonic stages. Examining tumor gene expression through the lens of development has revealed an extensive network of therapeutic targets for cancer control. Keywords: Tumors from four murine models of colorectal cancer and normal mouse colon samples at different developmental stages
Project description:Fluorescence-activated cell sorting (FACS) was used to separate colon tumor samples into two fractions of ALDH Negative and ALDH Positive cells using the Aldefluor Assay. RNA samples were derived from FAC-sorted 3D in-vitro models of patient-derived colon tumors. Samples from unfractionated in vitro models are also included.