z-logo
open-access-imgOpen Access
Identification of microRNAs targeting NAT1 and NAT2 gene transcripts in prostate cancer patients observed in different races
Author(s) -
David Agustriawan,
Arli Aditya Parikesit,
Rizky Nurdiansyah,
Kevin Nathanael Ramanto
Publication year - 2019
Publication title -
iop conference series. materials science and engineering
Language(s) - English
Resource type - Journals
eISSN - 1757-899X
pISSN - 1757-8981
DOI - 10.1088/1757-899x/546/6/062017
Subject(s) - microrna , prostate cancer , gene , in silico , biology , cancer , lung cancer , oncology , prostate , medicine , cancer research , genetics
Prostate cancer has the second highest death rate second only to lung cancer. Mutation in a single gene does not cause prostate cancer. Instead, many different genes are responsible, including NAT1 and NAT2 gene. By finding microRNAs that can suppress NAT1 and NAT2 gene, a novel prostate cancer treatment can be developed. Prostate cancer is also more commonly found in African-American than White-American. Therefore, this in silico study aimed to find several microRNAs targeting NAT1 and NAT2 gene observed in black, white, and other racial groups. 100 white patients, 100 races not reported patients, 11 black patients, and 638 combined races patient’s expression data were collected with TCGA-Assembler in R from The Cancer Genomic Atlas (TCGA). Next, Spearman correlation analysis was performed in R to find microRNAs that are negatively correlated with NAT1 and NAT2 gene. MicroRNAs were validated with miRTarBase and RNAhybrid. Only microRNAs which are located in combined patients and found in at least another race group is considered, i.e., hsa-mir-103a-1, hsa-mir-183, hsa-mir-32, and hsa-mir-96. Race-specific microRNA cannot be determined due to small sample size in black race group. Further study is needed to confirm the interaction between listed microRNAs with NAT1 and NAT2 gene expressions.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here