Title |
Deciphering the Role of microRNAs in BRD4-NUT Fusion Gene Induced NUT Midline Carcinoma |
Authors |
Ekta Pathak1, Bhavya1, Divya Mishra1, Neelam Atri1,2, Rajeev Mishra1*
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Affiliation |
1Bioinformatics Department, MMV, Banaras Hindu University, India; 2Botany Section, MMV, Banaras Hindu University, India;
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mishrarajeev@gmail.com; rajeev17@bhu.ac.in
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Article Type |
Hypothesis
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Date |
Received May 19, 2017; Accepted June 5, 2017; Published June 30, 2017
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Abstract |
NUT midline carcinoma (NMC) is a very aggressive and lethal type of squamous epithelial cell cancer caused due to fusion of BRD4 and NUT genes. The gene fusion results into a new fusion protein that promotes oncogenesis. The detailed molecular mechanisms underlying the NMC are still not clear and new findings are urgently required to complement the current efforts. Abnormal microRNAs (miRNA) expression promotes tumour formation by modulating the functional expression of critical genes other than the parent genes involved in tumour cell proliferation or survival. Here, using Insilco methods, miRNA targeting the transcripts of parent genes (BRD4 and NUT) and the BRD4-NUT fusion gene were predicted. We investigated a situation, wherein abnormal miRNA expression in malignant cells could arise due to deletion and fusion of genomic regions encompassing the target site of miRNA genes. A set of 48 dysregulated miRNAs targeting the critical genes other than the parent genes (BRD4 and NUT) was identified. Functional enrichment analysis of KEGG pathways of target genes of these Ex-miRNAs implicates their role in cancer pathways. Amplification in the expression level of these miRNAs can be used for NMC diagnosis and prognosis.
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Keywords |
microRNAs, BRD4-NUT, Fusion Gene, NUT midline carcinoma, bioinformatics approach
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Citation |
Pathak et al. Bioinformation 13(6): 209-213 (2017)
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Edited by |
P Kangueane
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ISSN |
0973-2063
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Publisher |
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License |
This is an Open Access article which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. This is distributed under the terms of the Creative Commons Attribution License.
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