Involvement of MIR4301 in the DRD2 mediated tumor growth by in-silico analysis

سال انتشار: 1395
نوع سند: مقاله کنفرانسی
زبان: انگلیسی
مشاهده: 434

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شناسه ملی سند علمی:

IPMCMED01_114

تاریخ نمایه سازی: 23 آذر 1397

چکیده مقاله:

Background: Various types of neoplasms including breast cancer exhibit of different profile changes in both mRNA and micro-RNA expression. The dopamine receptors are dysregulated in various human cancers, but the molecular mechanisms underlying dopamine receptors mediated tumor growth remain unclear. Here we examined the involvement of MIR4301 in the DRD2 mediated tumor growth by in-silico analysis.Methods: To determine the gene targets of the differentially expressed miRNAs, we used three of the leading miRNA target prediction algorithms: mirwalk2, PicTar, and TargetScan. Mirwalk2 found the miRNA-target genes in the Carcinogenesis pathway and verified by KEGG pathways. KEGG pathway is derived from Kanehisa Lab, Kyoto University, Japan. This analysis is used to determine the position and role of this MIR4301 in controling carcinogenesis pathway. The position and function of genes in a pathway are crucial for recognizing the mechanism of intervention or regulation of MIR4301 in carcinogenesis.We aligned DRD2 (ENST00000362072) and MIR4301 in NCBI database and found that this MIR located within the DRD2 intronic region. Structural and stability analysis of MIR4301 was conducted by using the online application Mfold.Results: By using three target prediction tools, 9882 candidate genes were predicted for MIR4301 and all the predicted candidate genes were analyzed by pathways enriched analysis. KEGG and Panther pathways enrichment analysis showed that 36417 endometriosis-related miRNA targets were mainly cancer-related pathways RAS and PI3K pathway.Conclusions: MIR 4301 is a 65 base-pair long non-coding RNA localized in chromosome 11 (nt: 113450023-113450088). Bioinformatics analysis has showed, DRD2 can be a potential target of MIR4301and suggested the probable effect of this microRNA in the regulation of DRD2 expression.

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نویسندگان

Naghmeh Gholipour

national institute of genetic engineering and biotechnology (nigeb), tehran, iran

Ghasem Ahangari

national institute of genetic engineering and biotechnology (nigeb), tehran, iran