Study of the transcriptional effect of ANO1 knock-down in two head and neck squamous cell carcinoma cell lines by RNA-sequencing of samples cultured in three dimensional collagen type I
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE163639 | GEO | 2021/03/10
REPOSITORIES: GEO
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Project description:PPFIA1 (encodes for liprin-α1) locates at the commonly amplified 11q13 region in cancer, but the precise mechanism of liprin-α1 function has remained unclear. In this study we show how genes are differentially expressed after liprin-α1 knockdown in different cell lines, grown in three dimensional matrix. The overall goal was to gain insight into the mechanism by which liprin-α1 has an effect on the progression of head and neck carcinomas and breast carcinomas in three dimensional environment.
2018-07-19 | GSE108392 | GEO
Project description:OBJECTIVES: Amplification of the 11q13 locus is commonly observed in a number of human cancers including both breast and ovarian cancer. Cyclin D1 and EMS1 have been implicated as candidate oncogenes involved in the emergence of amplification at this locus. Detailed analysis of the 11q13 amplicon in breast cancer led to the discovery of four regions of amplification suggesting the involvement of other genes. Here, we investigate the role of EMSY, a recently described BRCA2 interacting protein, as a key element of the 11q13 amplicon in ovarian cancer. EMSY maps to 11q13.5 and is amplified in 13% of breast and 17% of ovarian carcinomas. METHODS: EMSY amplification was assessed by fluorescent in-situ hybridization (FISH) in 674 ovarian cancers in a tissue microarray and correlated with histopathological subtype and tumor grade. A detailed map of the 11q13 amplicon in 51 cases of ovarian cancer was obtained using cDNA-array-based comparative genomic hybridization (aCGH). To further characterize the role of EMSY within this amplicon, we evaluated both the amplification profiles and RNA expression levels of EMSY and two other genes from the 11q13 amplicon in an additional series of 22 ovarian carcinomas. : EMSY amplification was seen in 52/285 (18%) high grade papillary serous carcinomas, 4/27 (15%) high grade endometrioid carcinomas, 3/38 (8%) clear cell carcinomas, and 3/10 (30%) undifferentiated carcinomas. aCGH mapping of 11q13 in ovarian cancer showed that EMSY localized to the region with the highest frequency of copy number gain. Cyclin D1 and EMS1 showed a lower frequency of copy number gain. A highly significant correlation between EMSY gene amplification and RNA expression was also observed (P = 0.0001). This was a stronger correlation than for other genes at 11q13 including Cyclin D1 and PAK1. CONCLUSIONS: These findings support the role of EMSY as a key oncogene within the 11q13 amplicon in ovarian cancer. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set Using regression correlation
2010-06-25 | E-GEOD-16408 | biostudies-arrayexpress
Project description:OBJECTIVES: Amplification of the 11q13 locus is commonly observed in a number of human cancers including both breast and ovarian cancer. Cyclin D1 and EMS1 have been implicated as candidate oncogenes involved in the emergence of amplification at this locus. Detailed analysis of the 11q13 amplicon in breast cancer led to the discovery of four regions of amplification suggesting the involvement of other genes. Here, we investigate the role of EMSY, a recently described BRCA2 interacting protein, as a key element of the 11q13 amplicon in ovarian cancer. EMSY maps to 11q13.5 and is amplified in 13% of breast and 17% of ovarian carcinomas. METHODS: EMSY amplification was assessed by fluorescent in-situ hybridization (FISH) in 674 ovarian cancers in a tissue microarray and correlated with histopathological subtype and tumor grade. A detailed map of the 11q13 amplicon in 51 cases of ovarian cancer was obtained using cDNA-array-based comparative genomic hybridization (aCGH). To further characterize the role of EMSY within this amplicon, we evaluated both the amplification profiles and RNA expression levels of EMSY and two other genes from the 11q13 amplicon in an additional series of 22 ovarian carcinomas. : EMSY amplification was seen in 52/285 (18%) high grade papillary serous carcinomas, 4/27 (15%) high grade endometrioid carcinomas, 3/38 (8%) clear cell carcinomas, and 3/10 (30%) undifferentiated carcinomas. aCGH mapping of 11q13 in ovarian cancer showed that EMSY localized to the region with the highest frequency of copy number gain. Cyclin D1 and EMS1 showed a lower frequency of copy number gain. A highly significant correlation between EMSY gene amplification and RNA expression was also observed (P = 0.0001). This was a stronger correlation than for other genes at 11q13 including Cyclin D1 and PAK1. CONCLUSIONS: These findings support the role of EMSY as a key oncogene within the 11q13 amplicon in ovarian cancer. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set
2009-06-04 | GSE16408 | GEO
Project description:Background: The amplification event occurring at chromosome locus 11q13, reported in several different cancers, includes a number of potential oncogenes. We have previously reported amplification of one such oncogene, CCND1, to be correlated with an adverse effect of tamoxifen in premenopausal breast cancer patients. Overexpression of cyclin D1 protein however, confers tamoxifen resistance but not a tamoxifen induced adverse effect. Potentially, co-amplification of an additional 11q13 gene, with a resulting protein overexpression, is required to cause an agonistic effect. Moreover, during 11q13 amplification a deletion of the distal 11q region has been described. In order to assess the potential impact of the deletion we have examined a selected marker for this event. Methods: Array CGH analysis was employed to identify and confirm changes in the gene expression of a number of different genes mapping to the 11q chromosomal region, associated with CCND1 amplification. The subsequent protein expression of these candidate genes was then examined in a clinical material of 500 primary breast cancers from premenopausal patients randomized to either tamoxifen or no adjuvant treatment. The protein expression was also compared to the CGH data in a subset of 56 breast cancer samples. Results: Cortactin and FADD overexpression was linked to CCND1 amplification, determined by FISH, but was not associated with a diminished effect of tamoxifen. However, deletion of distal chromosome 11q, defined as downregulation of the marker Chk1, was associated with an impaired tamoxifen response, and interestingly, also with low proliferative breast cancer of low grade. For Pak1 and cyclin D1 the protein expression corresponded to the gene expression data from the CGH analysis. Conclusions: The results indicate that many 11q13 associated gene products are overexpressed in conjunction with cyclin D1 but not linked to an agonistic effect of tamoxifen. Finally, the deletion of distal 11q, linked to 11q13 amplification, might be an important event affecting breast cancer outcome and tamoxifen response. Keywords: comparative genomic hybridisation 56 samples with 11q13 amplification have been analysed and compared with protein expression results from immunohistochemical analyses.
2008-10-07 | E-GEOD-12759 | biostudies-arrayexpress
Project description:Alternative splicing of pre-mRNA generates protein diversity and has been linked to cancer progression and drug response. Exon microarray technology enables genome-wide quantication of expression levels for the majority of exons and facilitates the discovery of alternative splicing events. Analysis of exon array data is more challenging than gene expression data and there is a need for reliable quantication of exons and alternative spliced variants. We introduce a novel, computationally efficient methodology, MEAP, for exon array data preprocessing, analysis and visualization. We compared MEAP with other preprocessing methods, and validation of the results show that MEAP produces reliable quantication of exons and alternative spliced variants. Analysis of data from head and neck squamous cell carcinoma (HNSCC) cell lines revealed several variants associated with 11q13 amplication, which is a predictive marker of metastasis and decreased survival in HNSCC patients. Together these results demonstrate the utility of MEAP in suggesting novel experimentally testable predictions. Thus, in addition to novel methodology to process large-scale exon array data sets, our results provide several HNSCC candidate genes for further studies. We analyzed 15 samples using the Affymetrix Human Exon 1.0 ST platform, of which 7 samples have 11q13 amplification. Array data was preprocessed by using Multiple Exon Array Processing (MEAP).
2011-06-10 | E-GEOD-27501 | biostudies-arrayexpress
Project description:Aberrant activation of Wnt beta-catenin signalling is a major driving force in colon cancer. Wnt beta-catenin signalling induces the expression of the transcription factor c-Myc, leading to cell proliferation and tumourigenesis. c-Myc regulates multiple biological processes through its ability to directly modulate gene expression. However, the mechanisms underlying c-Myc-induced oncogenesis remain to be established. Here we identify a novel direct target of c-Myc, MYU (c-Myc-upregulated long non-coding RNA) and show that MYU is upregulated in most colon cancers and is required for the tumourigenicity of colon cancer cells. We further demonstrate that MYU associates with the RNA-binding protein hnRNP-K to stabilize CDK6 expression, and thereby promotes the G1-S transition of the cell cycle. These results suggest that the MYU/hnRNP-K/CDK6 pathway functions downstream of Wnt/c-Myc signalling and plays a critical role in the proliferation and tumourigenicity of colon cancer cells. MYU might be a promising molecular target for the therapeutic treatment of c-Myc-driven cancers.
2016-09-10 | GSE64889 | GEO
Project description:Background: The amplification event occurring at chromosome locus 11q13, reported in several different cancers, includes a number of potential oncogenes. We have previously reported amplification of one such oncogene, CCND1, to be correlated with an adverse effect of tamoxifen in premenopausal breast cancer patients. Overexpression of cyclin D1 protein however, confers tamoxifen resistance but not a tamoxifen induced adverse effect. Potentially, co-amplification of an additional 11q13 gene, with a resulting protein overexpression, is required to cause an agonistic effect. Moreover, during 11q13 amplification a deletion of the distal 11q region has been described. In order to assess the potential impact of the deletion we have examined a selected marker for this event. Methods: Array CGH analysis was employed to identify and confirm changes in the gene expression of a number of different genes mapping to the 11q chromosomal region, associated with CCND1 amplification. The subsequent protein expression of these candidate genes was then examined in a clinical material of 500 primary breast cancers from premenopausal patients randomized to either tamoxifen or no adjuvant treatment. The protein expression was also compared to the CGH data in a subset of 56 breast cancer samples. Results: Cortactin and FADD overexpression was linked to CCND1 amplification, determined by FISH, but was not associated with a diminished effect of tamoxifen. However, deletion of distal chromosome 11q, defined as downregulation of the marker Chk1, was associated with an impaired tamoxifen response, and interestingly, also with low proliferative breast cancer of low grade. For Pak1 and cyclin D1 the protein expression corresponded to the gene expression data from the CGH analysis. Conclusions: The results indicate that many 11q13 associated gene products are overexpressed in conjunction with cyclin D1 but not linked to an agonistic effect of tamoxifen. Finally, the deletion of distal 11q, linked to 11q13 amplification, might be an important event affecting breast cancer outcome and tamoxifen response. Keywords: comparative genomic hybridisation
2008-10-08 | GSE12759 | GEO
Project description:In order to gain insight into epithelial morphogenesis and the influence of culture geometry on gene expression patterns, Madin Darby Canine Kidney (MDCK) epithelial cells where grown in 2-dimensional (2D) culture or 3-dimensional (3D) culture . MDCK cells cultured in 2D were plated atop a pre-solidified type I collagen gel. Cells cultured under these conditions grew as flat monolayer sheets. In 3D culture, cells are embedded within type I collagen gel. Cells grown under these conditions form large spherical cysts with hollow central lumens. We anticipate, therefore, that these results provide insight into the mechanisms that regulate epithelial cystogenesis. Cells grown in the 2D or 3D geometries were collected from digested type I collagen gels on day 8. The 2D MDCK cells were treated as the control condition and there gene expression patterns were compared to those of 3D grown cells, which served as the experimental condition.
2013-06-03 | E-GEOD-28381 | biostudies-arrayexpress
Project description:To determine which signalling pathways are affected by small RNAs (piRNAs, miRNAs) through target regulation in Glioblastoma Multiforme (GBM), we performed high-throughput next-generation sequencing in U87-MG GBM cell line. The RNA sequencing (RNA-Seq) of small RNAs and transcriptomes discovered both known and novel piRNAs and miRNAs as well other transcriptomes of protein-coding genes, lncRNAs and pseudogenes expressed in this GBM cell line. These small RNAs and target transcriptomes can be further investigated to decode novel molecular mechanisms underlying oncogenesis of this malignancy.
2023-04-04 | GSE197508 | GEO
Project description:RNA seq analysis was performed to assess the transcriptional profiles of BxPC3 cells with different status of ANO1 and KRAS.
2023-03-31 | GSE202825 | GEO