UTP18 as an oncogene promotes colorectal adenoma to carcinoma progression
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE142023 | GEO | 2020/05/01
REPOSITORIES: GEO
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Project description:Colorectal cancer often develops slowly from adenoma. In this study, we aimed to identify the oncogenes involved in the progression of colorectal adenoma to carcinoma by Tandem Mass Tag (TMT)-based quantitative proteomics. Protein expression changes were compared by TMT-based quantitative mass spectrometry in seven paired samples of normal mucosa, adenoma and carcinoma. Moreover, a bioinformatics analysis of differential protein expression was performed to screen for oncogenes. Effects of oncogene knockdown on cell viability, proliferation, migration and invasion were analyzed in colorectal cancer cell lines. Effects of oncogene overexpression on cell viability and proliferation were analyzed in adenoma organoids. The protein UTP18 was consistently upregulated in the normal-adenoma-carcinoma sequence. UTP18 downregulation was shown to inhibit colorectal cancer cell viability, proliferation, migration and invasion. UTP18 overexpression promoted adenoma organoid viability and proliferation. UTP18 facilitated the expression of MYC and impaired expression of the tumor-suppressor p21. Our data revealed the importance of UTP18 as an effector in the progression of adenoma to carcinoma. Thus, UTP18 is implicated as a highly specific biomarker for early diagnosis of progressive adenomas.
2020-06-01 | PXD017068 |
Project description:UTP18 as an oncogene promotes colorectal adenoma to carcinoma progression
| PRJNA595591 | ENA
Project description:Chromosomal instability (CIN) is the hallmark of colorectal adenoma to carcinoma progression in 85% of cases, with 20q gain as the most prominent aberration. Yet, the oncogenes at this chromosomal gain are still largely unknown. Here, we aimed to identify oncogenes at 20q involved in colorectal adenoma to carcinoma progression by measuring the effect of 20q gain on gene expression in this amplicon. Segmentation of DNA copy number changes on 20q was performed by array CGH in 67 colorectal adenomas and carcinomas. Additionally, robust analysis of mRNA expression in these segments was performed in 68 adenomas and carcinomas. This approach revealed seven genes to be important in CIN related adenoma to carcinoma progression. These genes may both serve as highly specific biomarkers for presence of high-risk precursor lesions as well as potential targets for pharmaceutical intervention. Keywords: Integration of array CGH and expression microarrays in colorectal cancer progression
2008-10-15 | GSE8067 | GEO
Project description:Chromosomal instability (CIN) is the hallmark of colorectal adenoma to carcinoma progression in 85% of cases, with 20q gain as the most prominent aberration. Yet, the oncogenes at this chromosomal gain are still largely unknown. Here, we aimed to identify oncogenes at 20q involved in colorectal adenoma to carcinoma progression by measuring the effect of 20q gain on gene expression in this amplicon. Segmentation of DNA copy number changes on 20q was performed by array CGH in 67 colorectal adenomas and carcinomas. Additionally, robust analysis of mRNA expression in these segments was performed in 68 adenomas and carcinomas. This approach revealed seven genes to be important in CIN related adenoma to carcinoma progression. These genes may both serve as highly specific biomarkers for presence of high-risk precursor lesions as well as potential targets for pharmaceutical intervention. Keywords: Integration of array CGH and expression microarrays in colorectal cancer progression We performed array CGH on a panel of 41 progressed adenomas, from which the adenoma and carcinoma components were separately analysed (total, 82 samples). The DNA obtained from these samples was extracted from formalin-fixed, paraffin-embedded material. Additionally we analysed a series of independent frozen adenomas and carcinomas by array CGH (34 adenomas and 33 carcinomas) and expression microarrays (37 adenomas and 31 carcinomas). For array-CGH we used as reference DNA for all samples, a pool of 10 normal individuals. For expression microarrays we used as reference a commercial available RNA (pool of different cancer cell lines), from Strategene. No replicates nor dye swaps were done.
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Project description:Colorectal cancer (CRC) remains a major cause of cancer related-death in developed countries. The risk of death is correlated with the stage of CRC determined at the primary diagnosis and early diagnosis is associated with enhanced survival rate. Consequently, there is an interest in using proteomics technologies to identify specific markers of adenomatous polyps as well as advanced stages of CRC.This study supports the concept that serum proteins can discriminate adenoma and CRC patients from unaffected patients and highlights the value of the SERPIN family as potential biomarkers of CRC.
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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.
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Project description:In the carcinogenesis of colorectal cancer (CRC), the stepwise progression from adenoma to carcinoma is marked by a series of specific genetic alterations of known oncogenes and tumor suppressor genes. However, many patient-matched features of the transcriptome involved in the adenoma-carcinoma sequence remain unidentified. The aim of this study was to identify genes associated with the process of CRC formation by analyzing the characteristics of the transcriptome during tumor formation. Six dynamic expression patterns specific to tumor formation were characterized for the first time. Dysregulation of metabolic pathways, suppression of the immune system, and activation of canonical pathways related to cancer were associated with the adenoma-carcinoma sequence. Among a cluster of genes positively correlated with tumor formation, TPD52L1 was identified as a gene that induced oncologic behaviors and a biomarker for poor prognosis.
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Project description:Abnormal DNA methylation is a hallmark of human cancers and may be a promising biomarker for early diagnosis of human cancers1. However, the majority of DNA methylation biomarkers that have been identified are based on the hypothesis that early differential methylation regions (DMRs) are maintained throughout carcinogenesis and could be detected at all stages of cancer. In this study, we identified potential early biomarkers of colorectal cancer (CRC) development by genome-wide DNA methylation assay (Illumina infinium450, 450K) to normal (N=20) and pre-colorectal cancer samples including 18 low-grade adenoma (LGA) and 22 high-grade adenoma (HGA).
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