Computational prediction of miRNA binding sites in mRNA of colorectal cancer candidate genes

Aigul Akimniyazova11SRI of Biology and Biotechnology problems, al-Farabi Kazakh National University, akimniyazova@gmail.com The identification of causative miRNAs in colorectal cancer is unclear due to a lack of understanding of how specific miRNAs affect biological pathways and consequences of disease development. The miRNA is a class of nano-sized non-coding RNAs that regulate many mRNAs, and mRNA can be related to many miRNAs, which make them suitable for diagnosis purposes. Therefore it is required to identify candidate genes of colorectal cancer and to what extent they can interact with miRNA. To determine the important miRNAs biding sites in genes, involved in the development of colorectal cancer, there were used the MirTarget program. The paper presents the results of studying the characteristics of the interaction of miRNAs with mRNAs of 135 candidate genes involved in the development of colorectal cancer. The binding sites of 446 miRNAs have in 113 mRNA of genes at 5\’UTR, CDS, and 3\’UTR. Found miRNA binding sites with overlapped nucleotide sequences (clusters). The research results are useful for the development of methods for early diagnosis of this disease.

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Consideration of pathogenicity of nsSNVs in CDKN2A gene, as a new tumor marker for leukemia, using bioinformatics methods

Poster (download) Video (download) Farzaneh Ghasemi1, Mohammad Mehdi Heidari2, Mehri Khatami3, Yuriy L. Orlov41Department of Biology, Faculty of science,Yazd University, Yazd, Iran, heidarimm@yazd.ac.ir2Department of Biology, Faculty of science,Yazd University, Yazd, Iran, heidarimm@yazd.ac.ir3Department of Biology, Faculty of science,Yazd University, Yazd, Iran, heidarimm@yazd.ac.ir4I.M.Sechenov First Moscow State Medical University, Moscow, Russia, orlov@bionet.nsc.ru CDKN2A as a tumor suppressor gene (TSG) encodes p14 and p16 that they are tumor suppressor proteins and cell cycle regulators. Downregulation of these proteins causes various cancers. Sequence deletions or promoter hypermethylation lead to downregulation of these proteins. Also, point mutations can be caused malfunction or dysfunction of proteins. The aim of this study is definition of pathogenicity of non-synonymous single nucleotide variants (nsSNVs). We study three nsSNVs including rs104894095, rs786204195 and rs104894098 from NCBI/dbSNP databank. Then, these nsSNVs are considered by bioinformatics tools such as SIFT, PolyPhen-2, I-Mutant2.0, PANTHER, P-Mut, ExPASy/ProtScale, PEPTIDE 2.0 web server and PyMOL software. Plot of hydrophobicity of rs104894098 (V126D) is significantly changed. Also, we study hydrogen bonds length and atom distances in Aspartic acid substituted Valine in position 126 by PyMOL software. These parameters are compared with wild type protein. Finally, we find that rs786204195 and rs104894095 have destructive effects. But, rs104894098 (V126D) is deleterious because polar contacts, protein stability and hydrophobicity are changed in mutant form. This theory should be proved with experimental studies.

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