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30 Jun 2024 (Vol 47 , Iss 06 )

Journal ID : TMJ-03-02-2022-11085
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Title : Study of combination effect the MALAT1-ncRNA and DNA CGIs-Methylation in Colorectal Cancer regression

Abstract :

Colorectal cancer is currently most frequent cancer type in oncologic pathology .It is a prevalent disease among the elderly .Non coding RNAs alter gene expression at nume-rous levels, including chromatin modification, transcription and post-transc-ription.LncRNAs are composed of more than200nucleotides without production of proteins.They are irregularly expressed in many cancer cells and play a key role in a number of cancer symptoms.DNA methylation is a critical epigenetic alteration that controls gene expression.The addition of methyl group to the 5carbon of cytosine residues in CpG dinucleotides is termed as DNA methylation. In mammalian genomes, CpG dinucleotides are dispersed irregularly, aggregating primarily in CGIs, which are frequently found within gene promoters region.The human col-orectal adenocarcinoma(CRC)cell lines HT29(ATCC®HTB-38),and nor-mal lung fibroblast cell line(ATCC® CCL-75)were utilized in this research for MALAT1 molecule transfection and CpGs-islands methylation.Cell co-unting was achieved by6-well plate and 24-well plate prior to transfection using hemocytometer. The two cell lines were transfected with MALAT1 antisensemolecule.Transfection efficiency, cell viability and target lcnRNA expression was conducted, then CGIs-methylation was achieved by bisulfate conversion.The present outcomes showed down regulation of oncogenes (KRAS and AKT1) and up regulation of TSGs(TP53 and KEAP1), in addition CpG-islands methylation showed significant methylation of oncogenes pro-moter region and unblocking of TSGs promoter region. The researchers concluded that analysis of interpretation outcomes of MALAT1-CGIs-meth-ylation led to inhibit of H29 cell line proliferation.

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