LncRNA and mRNA expression profile in colorectal adenoma and cancer
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ABSTRACT:
PROVIDER: PRJNA412450 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We evaluated the profile of lncRNA and mRNA expression in 6 colorectal adenoma (CRA), 6 colorectal adenoma (CRC) and 6 matched normal mucosa (NOR) using the Exiqon miRCURY lncRNA and mRNA array,7th generation. We found that global dysregulated lncRNA and mRNAs between colorectal lesions and normal mucosa. Our findings implicates that dysregulation of lncRNA and mRNAs may play important role in the carcinogenesis and present therapeutic targets for CRC.
2020-09-28 | GSE104364 | GEO
Project description:We evaluated the profile of miRNA expression in 6 colorectal adenoma (CRA), 6 colorectal adenocarcinoma (CRC) and 6 matched normal mucosa (NOR) using the Exiqon miRCURY LNA microRNA array,7th generation. We found that global dysregulated miRNAs between colorectal lesions and normal mucosa. Our findings implicates that dysregulation of miRNAs may play important role in the carcinogenesis and present therapeutic targets for CRC.
2018-08-23 | GSE72281 | GEO
Project description:We established human colorectal tumor organoids from benign adenoma, primary colorectal cancer or metastasized colorectal cancer. The gene signature of tumor organoids associated with their tumor progression status. We also generated genome-edited organoids from human intestinal organoids recapitulating adenoma-carcinoma sequence. Gene expression signature of the genome engineered organoids were similar to that of adenoma organoids. This result indicated multiple (up to five) genetic mutations were insufficient for gene expression reprogramming of colorectal cancer. We used microarrays to detail the global program of gene expression in human colorectal tumor organoids and artificially mutation introduced organoids.
2015-01-18 | GSE57965 | GEO
Project description:We established human colorectal tumor organoids from benign adenoma, primary colorectal cancer or metastasized colorectal cancer. The gene signature of tumor organoids associated with their tumor progression status. We also generated genome-edited organoids from human intestinal organoids recapitulating adenoma-carcinoma sequence. Gene expression signature of the genome engineered organoids were similar to that of adenoma organoids. This result indicated multiple (up to five) genetic mutations were insufficient for gene expression reprogramming of colorectal cancer. We used microarrays to detail the global program of gene expression in human colorectal tumor organoids and artificially mutation introduced organoids. To assess the expression profiling of genome-engineered organoids, we prepared total-RNA from cultured adenoma, carcinoma and genome-engineered organoids. We produced two types of genome-engineered organoids using the CRISPR/Cas9 or lentivirus vector system. Each engineered gene and engineered methods are described as a single alphabet and method name, respectively, in the sample characteristics field. The abbreviations for the engineered genes are as follows. 1) Genome-engineered organoids with CRISPR/Cas9 A = APC deletion; K = KRAS G12V knock in; S = Smad4 deletion; T = TP53 deletion; P = PIK3CA E545K knock in. 2) Genome-engineered organoids with Lent virus vector B = CTNNB1 S33Y overexpression; K = KRAS G12V overexpression; S = Smad4 shRNA overexpression; T = TP53 shRNA overexpression; P = PIK3CA E545K overexpression.
2015-01-18 | E-GEOD-57965 | biostudies-arrayexpress
Project description:Traditional serrated adenoma (TSA) remains the least understood of all the colorectal adenomas although these lesions have been associated with a significant cancer risk- twice that of the conventional adenoma (CAD) and of the sessile serrated adenoma (SSA/P). This study was performed to investigate the proteomic profiles of the different colorectal adenomas to better assess the pathogenesis of TSA. We performed a global quantitative expression profile of 44 colorectal adenomas (12 TSA, 15 CAD, 17 SSA/Ps) and 17 normal colonic mucosa, conserved as formalin-fixed paraffin-embedded samples, by the label-free quantification (LFQ) method. Unsupervised consensus hierarchical clustering applied to the whole proteomic profile of the 44 colorectal adenomas identified four subtypes. The C1 and C2 were well-individualized clusters composed of most of the CAD (14/15) and most of the SSA (13/17) respectively. This is consistent with the fact that CAD and SSA/Ps are homogeneous but distinct colorectal adenoma entities. In contrast, TSA were subdivided into C3 and C4 clusters that also contained CAD and SSA/Ps, consistent with the more heterogeneous entity of TSA at the morphological and molecular levels. The comparison of the proteome expression profile between the adenoma subtypes and normal colonic mucosa further confirmed the heterogeneous nature of TSA that merged either on CAD or SSA, while CAD and TSA formed homogeneous and distinct entities. Furthermore, we identified LEFTY1 a new potential marker for TSA that may be relevant for the TSA pathogenesis. LEFTY1 is an inhibitor of the Nodal/TGFb pathway that we found to be one of the most overexpressed proteins specifically in the TSA and confirmed by immunohistochemistry. Taken together, our study confirms that CAD and SSA form homogenous but distinct colorectal adenoma entities while TSA are an heterogeneous entity and may arise from either SSA or from normal mucosa that will evolve along the conventional adenoma pathway.
2020-01-21 | PXD014511 | Pride
Project description:We tried to examine whether the de novo colorectal carcinomas (CRCs) without an adenoma component can be discriminated from those deriving from adenoma by DNA copy-number alteration profile. The unsupervised clustering of DNA copy-number profiles of 112 colorectal cancer samples, using large-sized (≥ 9 probes) genes, disclosed 4 clusters: Clusters 1, 3, and 4 correspond to carcinoma with an adenoma component. Cluster 2 and some samples in cluster 3 correspond to carcinoma without adenoma component. Our approach suggested that Cluster 2 may represent de novo CRCs since penetrance plots were very different between cluster 2 and the other clusters. Adenocarcinoma in cluster 3 have higher potential for lymph node metastasis than those in cluster 1 and 4 and can derive from clusters 1/4 tumors.
2019-03-19 | GSE128433 | GEO
Project description:The differences in gene expression profile between adenoma and corresponding normal mucosa in colorectal cancer cases.
2005-05-20 | E-MEXP-341 | biostudies-arrayexpress
Project description:miRNA, mRNA and lncRNA expression in colorectal cancer
| PRJNA658911 | ENA
Project description:To determine the mRNA expression profile of colorectal cancer cell line HCT116 transfected with lncRNA-SPRY4-IT1 overexpression vector, we performedd gene expression microArray analysis to examine the expression of mRNAs.
2019-11-19 | GSE140616 | GEO
Project description:Approximately two decades ago, Vogelstein and Fearon proposed the adenoma-carcinoma sequence of sporadic CRC development and illustrated the accumulation of genetic alterations during the stepwise progression, thereby providing a guideline for clinical practice. Although the detection and excision of precancerous lesions could prevent colorectal cancer and reduce mortality, 6% of adenomas will ultimately develop into colorectal cancer. Thus, this genetic model for colorectal tumorigenesis may not completely reflect the complex essence of the disease and whether the mode of initiation of the events in the multistep progression affects the outcome of CRC is still unknown. In this study, mRNA and miRNA expression profiling was performed with human colorectal tissues, including normal mucosa, adenoma and adenocarcinoma. Then, an integrated approach was adopted to establish the regulatory interaction networks that were correlated with colorectal carcinogenesis. Finally, a 55-gene signature whose expression was down-regulated in precancerous lesions compared to normal tissue was identified as a potential early indicator of CRC survival. The results suggested that genes related to immunity and homeostasis played a critical role in protection against adenoma initiation and that the altered molecular events that influence colorectal cancer prognosis may be set in an early, precancerous stage.
2015-10-16 | GSE41657 | GEO