UTP18 as an oncogene promotes colorectal adenoma to carcinoma progression
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA595591 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10691629_1.fastq.gz | Fastqsanger.gz | |||
| SRR10691629_2.fastq.gz | Fastqsanger.gz | |||
| SRR10691630_1.fastq.gz | Fastqsanger.gz | |||
| SRR10691630_2.fastq.gz | Fastqsanger.gz |
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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.
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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
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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: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.
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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. Four types of human colorectal tissues were selected by colonoscopic resection or colorectal surgery, including 12 normal mucosae, 21 low-grade adenomas (mild or moderate atypical hyperplasia), 30 high-grade adenomas (severe atypical hyperplasia or carcinoma in situ) and 25 adenocarcinomas. Gene expression profiling analysis of these samples was performed using Agilent 4x44K human whole genome gene expression microarray (G4112F).
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