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Discovery of Long Non-Coding RNA MALAT1 Amplification in Precancerous Colorectal Lesions
A. Siskova, J. Kral, J. Drabova, K. Cervena, K. Tomasova, J. Jungwirth, T. Hucl, P. Kohout, S. Summerova, L. Vodickova, P. Vodicka, V. Vymetalkova
Jazyk angličtina Země Švýcarsko
Typ dokumentu časopisecké články
Grantová podpora
AZV NV18-03-00199
Grant Agency of the Ministry of Health of the Czech Republic
GACR 22-05942S
Grant Agency of the Czech Republic
Oncology and Haematology
Cooperatio Program
CZ.02.2.69/0.0/0.0/19_073 project n. START/MED/052
Grant Schemes project at UK
NLK
Free Medical Journals
od 2000
Freely Accessible Science Journals
od 2000
PubMed Central
od 2007
Europe PubMed Central
od 2007
ProQuest Central
od 2000-03-01
Open Access Digital Library
od 2000-01-01
Open Access Digital Library
od 2007-01-01
Health & Medicine (ProQuest)
od 2000-03-01
ROAD: Directory of Open Access Scholarly Resources
od 2000
PubMed
35887000
DOI
10.3390/ijms23147656
Knihovny.cz E-zdroje
- MeSH
- adenom * genetika patologie MeSH
- chromozomální nestabilita MeSH
- kolorektální nádory * genetika patologie MeSH
- lidé MeSH
- prekancerózy * genetika patologie MeSH
- RNA dlouhá nekódující * genetika MeSH
- srovnávací genomová hybridizace MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
A colorectal adenoma, an aberrantly growing tissue, arises from the intestinal epithelium and is considered as precursor of colorectal cancer (CRC). In this study, we investigated structural and numerical chromosomal aberrations in adenomas, hypothesizing that chromosomal instability (CIN) occurs early in adenomas. We applied array comparative genomic hybridization (aCGH) to fresh frozen colorectal adenomas and their adjacent mucosa from 16 patients who underwent colonoscopy examination. In our study, histologically similar colorectal adenomas showed wide variability in chromosomal instability. Based on the obtained results, we further stratified patients into four distinct groups. The first group showed the gain of MALAT1 and TALAM1, long non-coding RNAs (lncRNAs). The second group involved patients with numerous microdeletions. The third group consisted of patients with a disrupted karyotype. The fourth group of patients did not show any CIN in adenomas. Overall, we identified frequent losses in genes, such as TSC2, COL1A1, NOTCH1, MIR4673, and GNAS, and gene gain containing MALAT1 and TALAM1. Since long non-coding RNA MALAT1 is associated with cancer cell metastasis and migration, its gene amplification represents an important event for adenoma development.
Citace poskytuje Crossref.org
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