scholarly journals ADAMTS1, CRABP1, and NR3C1 Identified as Epigenetically Deregulated Genes in Colorectal Tumorigenesis

2006 ◽  
Vol 28 (5-6) ◽  
pp. 259-272 ◽  
Author(s):  
Guro E. Lind ◽  
Kristine Kleivi ◽  
Gunn I. Meling ◽  
Manuel R. Teixeira ◽  
Espen Thiis-Evensen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Colon Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cpg Island ◽  
Promoter Hypermethylation ◽  
Cancer Cell Lines ◽  
Colon Cancer Cell ◽  
Colorectal Carcinomas ◽  
Colon Cancer Cell Lines

Background: Gene silencing through CpG island hypermethylation is a major mechanism in cancer development. In the present study, we aimed to identify and validate novel target genes inactivated through promoter hypermethylation in colorectal tumor development. Methods: With the use of microarrays, the gene expression profiles of colon cancer cell lines before and after treatment with the demethylating agent 5-aza-2′-deoxycytidine were identified and compared. The expression of the responding genes was compared with microarray expression data of primary colorectal carcinomas. Four of these down-regulated genes were subjected to methylation-specific PCR, bisulphite sequencing, and quantitative gene expression analysis using tumors (n=198), normal tissues (n=44), and cell lines (n=30). Results: Twenty-one genes with a CpG island in their promoter responded to treatment in cell lines, and were simultaneously down-regulated in primary colorectal carcinomas. Among 20 colon cancer cell lines, hypermethylation was subsequently identified for three of four analyzed genes, ADAMTS1 (85%), CRABP1 (90%), and NR3C1 (35%). For the latter two genes, hypermethylation was significantly associated with absence or reduced gene expression. The methylation status of ADAMTS1, CRABP1, and NR3C1 was further investigated in 116 colorectal carcinomas and adenomas. Twenty-three of 63 (37%), 7/60 (12%), and 2/63 (3%) adenomas, as well as 37/52 (71%), 25/51 (49%), and 13/51 (25%) carcinomas were hypermethylated for the respective genes. These genes were unmethylated in tumors (n=82) from three other organs, prostate, testis, and kidney. Finally, analysis of normal colorectal mucosa demonstrated that the observed promoter hypermethylation was cancer-specific. Conclusion: By using a refined microarray screening approach we present three genes with cancer-specific hypermethylation in colorectal tumors, ADAMTS1, CRABP1, and NR3C1.

Methylation patterns ofIGFBP7 in colon cancer cell lines are associated with levels of gene expression

2007 ◽  
Vol 212 (1) ◽  
pp. 83-90 ◽  
Author(s):  
J Lin ◽  
M Lai ◽  
Q Huang ◽  
Y Ma ◽  
J Cui ◽  
...  
Keyword(s):  
Gene Expression ◽  
Colon Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Colon Cancer Cell ◽  
Colon Cancer Cell Lines ◽  
Methylation Patterns

scholarly journals Gene Expression Profile of Colon Cancer Cell Lines Treated with SN-38

Chemotherapy ◽  
2010 ◽  
Vol 56 (1) ◽  
pp. 17-25 ◽  
Author(s):  
Å. Wallin ◽  
P. Francis ◽  
M. Nilbert ◽  
J. Svanvik ◽  
X.-F. Sun
Keyword(s):  
Gene Expression ◽  
Colon Cancer ◽  
Gene Expression Profile ◽  
Cell Lines ◽  
Cancer Cell ◽  
Expression Profile ◽  
Cancer Cell Lines ◽  
Colon Cancer Cell ◽  
Colon Cancer Cell Lines

scholarly journals DNA methylation in the upstream CpG island of the GPER locus and its relationship with GPER expression in colon cancer cell lines

2020 ◽  
Author(s):  
Uttariya Pal ◽  
Sujasha Ghosh ◽  
Anil Mukund Limaye
Keyword(s):  
Dna Methylation ◽  
Colon Cancer ◽  
Estrogen Receptor ◽  
Cell Lines ◽  
Cancer Cell ◽  
Bisulfite Sequencing ◽  
Cpg Island ◽  
Cancer Cell Lines ◽  
Colon Cancer Cell ◽  
Colon Cancer Cell Lines

AbstractThe seven-transmembrane G-protein coupled estrogen receptor (GPER) relays short-term non-genomic responses in target cells and tissues. It is a proposed tumor suppressor, which frequently undergoes down-modulation in primary tumors of the breast, ovary, and endometrium. A study by Liu and co-workers reported the loss of GPER expression in colorectal cancer and attributed it to DNA methylation-dependent silencing. The present study is based on the hypothesis that GPER expression is inversely correlated with methylation in the upstream CpG island (upCpGi) in the GPER locus. Methylation in the upCpGi was analysed by bisulfite sequencing and correlated with GPER expression in a panel of colon cancer cell lines The bisulfite sequencing results show the presence of a differentially methylated region (DMR) comprising of the downstream eight CpGs of the upCpGi. Methylation in the DMR correlated inversely with GPER expression. We compared two cell lines, namely SW620 and COLO-320DM, in terms of their viability in response to varying concentrations of G1, a GPER specific agonist, which is known to induce cell cycle arrest and apoptosis in colon cancer cell lines. SW-620 cells, which had the least methylated DMR and the highest level of GPER expression, showed significant loss of viability with 1 μM G1. On the other hand, COLO-320DM, which had the most methylated DMR and the lowest level of GPER expression, did not show a significant response to 1 μM G1. At 5 μM G1, SW620 cells showed a greater reduction in viability than COLO-320DM cells. Our study demonstrates the inverse correlation between DNA methylation in the DMR and GPER expression. GPER is a non-canonical form of estrogen receptor, and estrogen is believed to exert its oncoprotective effect in the colon via GPER. DNA methylation-dependent silencing of GPER may, at least in part, the underlying reason behind the loss of estrogen’s oncoprotective effect in the colon. Future studies should explore the utility of DNA methylation in the upCpGi, particularly the DMR, in diagnosis or prognosis.

scholarly journals Insulin, CCAAT/Enhancer-Binding Proteins and Lactate Regulate the Human 11β-Hydroxysteroid Dehydrogenase Type 2 Gene Expression in Colon Cancer Cell Lines

PLoS ONE ◽  
2014 ◽  
Vol 9 (8) ◽  
pp. e105354 ◽  
Author(s):  
Thomas Andrieu ◽  
Pierre Fustier ◽  
Rasoul Alikhani-Koupaei ◽  
Irena D. Ignatova ◽  
Andreas Guettinger ◽  
...  
Keyword(s):  
Gene Expression ◽  
Colon Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Binding Proteins ◽  
Hydroxysteroid Dehydrogenase ◽  
Cancer Cell Lines ◽  
Colon Cancer Cell ◽  
Colon Cancer Cell Lines

scholarly journals Silencing LRH-1 in colon cancer cell lines impairs proliferation and alters gene expression programs

2015 ◽  
Vol 112 (8) ◽  
pp. 2467-2472 ◽  
Author(s):  
James R. Bayrer ◽  
Sridevi Mukkamala ◽  
Elena P. Sablin ◽  
Paul Webb ◽  
Robert J. Fletterick
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Colon Cancer ◽  
Cell Line ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Colon Cancer Cell ◽  
Colon Cancer Cell Lines ◽  
A Cell

Colorectal cancers (CRCs) account for nearly 10% of all cancer deaths in industrialized countries. Recent evidence points to a central role for the nuclear receptor liver receptor homolog-1 (LRH-1) in intestinal tumorigenesis. Interaction of LRH-1 with the Wnt/β-catenin pathway, highly active in a critical subpopulation of CRC cells, underscores the importance of elucidating LRH-1’s role in this disease. Reduction of LRH-1 diminishes tumor burden in murine models of CRC; however, it is not known whether LRH-1 is required for tumorigenesis, for proliferation, or for both. In this work, we address this question through shRNA-mediated silencing of LRH-1 in established CRC cell lines. LRH-1 mRNA knockdown results in significantly impaired proliferation in a cell line highly expressing the receptor and more modest impairment in a cell line with moderate LRH-1 expression. Cell-cycle analysis shows prolongation of G0/G1 with LRH-1 silencing, consistent with LRH-1 cell-cycle influences in other tissues. Cluster analysis of microarray gene expression demonstrates significant genome wide alterations with major effects in cell-cycle regulation, signal transduction, bile acid and cholesterol metabolism, and control of apoptosis. This study demonstrates a critical proproliferative role for LRH-1 in established colon cancer cell lines. LRH-1 exerts its effects via multiple signaling networks. Our results suggest that selected CRC patients could benefit from LRH-1 inhibitors.

scholarly journals Analysis of Cross-Association between mRNA Expression and RNAi Efficacy for Predictive Target Discovery in Colon Cancers

Cancers ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3091
Author(s):  
Euna Jeong ◽  
Yejin Lee ◽  
Youngju Kim ◽  
Jieun Lee ◽  
Sukjoon Yoon
Keyword(s):  
Gene Expression ◽  
Colon Cancer ◽  
Mrna Expression ◽  
Cell Lines ◽  
Cancer Cell ◽  
Large Scale ◽  
Cancer Cell Lines ◽  
Colon Cancer Cell ◽  
Transcriptional Networks ◽  
Colon Cancer Cell Lines

The availability of large-scale, collateral mRNA expression and RNAi data from diverse cancer cell types provides useful resources for the discovery of anticancer targets for which inhibitory efficacy can be predicted from gene expression. Here, we calculated bidirectional cross-association scores (predictivity and descriptivity) for each of approximately 18,000 genes identified from mRNA and RNAi (i.e., shRNA and sgRNA) data from colon cancer cell lines. The predictivity score measures the difference in RNAi efficacy between cell lines with high vs. low expression of the target gene, while the descriptivity score measures the differential mRNA expression between groups of cell lines exhibiting high vs. low RNAi efficacy. The mRNA expression of 90 and 74 genes showed significant (p < 0.01) cross-association scores with the shRNA and sgRNA data, respectively. The genes were found to be from diverse molecular classes and have different functions. Cross-association scores for the mRNA expression of six genes (CHAF1B, HNF1B, HTATSF1, IRS2, POLR2B and SATB2) with both shRNA and sgRNA efficacy were significant. These genes were interconnected in cancer-related transcriptional networks. Additional experimental validation confirmed that siHNF1B efficacy is correlated with HNF1B mRNA expression levels in diverse colon cancer cell lines. Furthermore, KIF26A and ZIC2 gene expression, with which shRNA efficacy displayed significant scores, were found to correlate with the survival rate from colon cancer patient data. This study demonstrates that bidirectional predictivity and descriptivity calculations between mRNA and RNAi data serve as useful resources for the discovery of predictive anticancer targets.

Studies of gene expression patterns in RER+ and RER- colon cancer cell lines

1998 ◽  
Vol 26 (3) ◽  
pp. S266-S266
Author(s):  
Donncha Dunican ◽  
Orna Tighe ◽  
Anne Parle-McDermott ◽  
David T. Croke
Keyword(s):  
Gene Expression ◽  
Colon Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Expression Patterns ◽  
Cancer Cell Lines ◽  
Colon Cancer Cell ◽  
Gene Expression Patterns ◽  
Colon Cancer Cell Lines
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