Project description:To determine the lncRNA expression profile in ectopic APC overexpressed CRC cell lines and control cells, we uesed lncRNA microArray analysis form Arraystar to examine lncRNA expression profile in ectopic APC overexpressed CRC cell lines and control cells.
Project description:ArrayStar Human LncRNA/mRNA Expression Microarray Version 3.0 was used to detect lncRNA expression in CRC tissues compared with their matched non-tumoral tissues. Here we report significantly up-regulated as well as down-regulated lncRNAs in CRC tissues compared with their matched non-tumoral tissues.
Project description:The purpose of this study is to identify lncRNAs involved in the pathology of colorectal cancer (CRC) progression and investigate their underlying mechanisms. The differentially expressed lncRNAs were identified between 15 CRC tissues and 15 adjacent normal tissues by Arraystar lncRNA microarrays
Project description:The purpose of this study is to identify lncRNAs involved in the pathology of colorectal cancer (CRC) liver metastasis and investigate their underlying mechanisms. A total of 439 miRNAs were identified to be differentially expressed between 7 primary CRC tissues with liver metastases and 8 CRC tissues without liver metastases from 15 patients by Arraystar lncRNA microarrays
Project description:Gene expression profiles were generated for CRC cell line SW1116 overexpressed POLR1D and empty vector to explore the effect of POLR1D on colorectal cancer cell line SW1116.
Project description:A collection of genetically engineered mouse models (GEMM) of colorectal cancer (CRC) were created, and primary tumors from these GEMMs were analyzed. Primary CRC tumors from these GEMMs were genotyped to confirm that they contain the core genetic lesions of interest, including APC, P53, KRAS, and BRAF. Primary tumors from GEMMs with combinations of lesions of interest were analyzed by whole genome expression, and their expression profiles were compared to determine how they segregate. Signatures were then generated from GEMM tumors of interest and compared to human clinical datasets with expression and outcome data. Primary tumors from CRC GEMMs with different combinations of mutant alleles of interested were generated and analyzed. Alleles include mutant forms of APC (A), P53 (P), KRAS (K) and BRAF (B).
Project description:The Adenomatous Polyposis Coli (APC) tumor suppressor is mutated in the vast majority of human colorectal cancers (CRC) and leads to deregulated Wnt signaling. To determine whether Apc disruption is required for tumor maintenance, we developed a mouse model of CRC whereby Apc can be conditionally suppressed using a doxycycline-regulated shRNA. Apc suppression produces adenomas in both the small intestine and colon that, in the presence of Kras and p53 mutations, can progress to invasive carcinoma. In established tumors, Apc restoration drives rapid and widespread tumor-cell differentiation and sustained regression without relapse. Tumor regression is accompanied by the re-establishment of normal crypt-villus homeostasis, such that once aberrantly proliferating cells reacquire self-renewal and multi-lineage differentiation capability. Our study reveals that CRC cells can revert to functioning normal cells given appropriate signals, and provide compelling in vivo validation of the Wnt pathway as a therapeutic target for treatment of CRC Analysis of RNA isolated from colon polyps that presented in shAPC or shAPC/Kras mice as compared to shRenilla (neutral) mouse colon mucosa
Project description:To identify the lncRNA profiles of colorectal carcinoma cells treated with aspirin, we performed microarray analysis using primary cultured cancer cells obtained from 8 clinical CRC tissues. After the CRC cells were treated with aspirin for 48 hours, 28 lncRNAs were statistically up-regulated more than 2-fold. We treated the primary cultured cancer cells obtained from 8 clinical CRC tissues with DMSO (negative control group_Rep8) and aspirin (Experiment group_Rep8).