Understanding the nucleotide composition and patterns of codon usage in the expression of human oral cancer genes

IF 1.5 4区 医学 Q4 BIOTECHNOLOGY & APPLIED MICROBIOLOGY
Tarikul Huda Mazumder , Arif Uddin
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引用次数: 0

Abstract

Oral squamous cell carcinoma (OSCC) is primarily known as oral cancer (OC) that mostly occurs in mouth, lips and tongue. Mutations in some of the genes cause OC and some genes are risk factors for progression of OC. In this study, we analyzed the compositional features and pattern of codon usage in genes involved in OC using computational method as no work was reported yet. Compositional features suggested that the overall GC content was higher i.e. genes were GC rich. Effective number of codons (ENC) values ranged from 34.6 to 55.9 with a mean value of 49.03±4.22 representing low codon usage bias (CUB). Correspondence analysis (COA) suggested that the codon usage pattern was different in different genes. In genes associated with OC, highly significant correlation was observed between GC12 and GC3 (r=0.454, p<0.01) suggesting that directional mutation affected all the three codon positions. This is the first report on pattern of codon usage pattern on genes involved in OC, which not only alludes a new perspective for elucidating the mechanisms of biased usage of synonymous codons but also provide valuable clues for molecular genetic engineering.

了解人类口腔癌基因表达中的核苷酸组成和密码子使用模式
口腔鳞状细胞癌(OSCC)主要称为口腔癌(OC),多发于口腔、嘴唇和舌头。有些基因突变会导致口腔鳞状细胞癌,有些基因则是口腔鳞状细胞癌恶化的危险因素。在本研究中,我们利用计算方法分析了 OC 相关基因的组成特征和密码子使用模式。组成特征表明,基因的整体 GC 含量较高,即富含 GC。有效密码子数(ENC)值在 34.6 至 55.9 之间,平均值为 49.03±4.22,代表低密码子使用偏差(CUB)。对应分析(COA)表明,不同基因的密码子使用模式不同。在与 OC 相关的基因中,观察到 GC12 和 GC3 之间存在高度显著的相关性(r=0.454,p<0.01),表明定向突变影响了所有三个密码子位置。这是首次报道涉及 OC 基因的密码子使用模式,不仅为阐明同义密码子的偏向使用机制提供了新的视角,而且为分子遗传工程提供了有价值的线索。
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来源期刊
CiteScore
4.90
自引率
0.00%
发文量
24
审稿时长
51 days
期刊介绍: Mutation Research (MR) provides a platform for publishing all aspects of DNA mutations and epimutations, from basic evolutionary aspects to translational applications in genetic and epigenetic diagnostics and therapy. Mutations are defined as all possible alterations in DNA sequence and sequence organization, from point mutations to genome structural variation, chromosomal aberrations and aneuploidy. Epimutations are defined as alterations in the epigenome, i.e., changes in DNA methylation, histone modification and small regulatory RNAs. MR publishes articles in the following areas: Of special interest are basic mechanisms through which DNA damage and mutations impact development and differentiation, stem cell biology and cell fate in general, including various forms of cell death and cellular senescence. The study of genome instability in human molecular epidemiology and in relation to complex phenotypes, such as human disease, is considered a growing area of importance. Mechanisms of (epi)mutation induction, for example, during DNA repair, replication or recombination; novel methods of (epi)mutation detection, with a focus on ultra-high-throughput sequencing. Landscape of somatic mutations and epimutations in cancer and aging. Role of de novo mutations in human disease and aging; mutations in population genomics. Interactions between mutations and epimutations. The role of epimutations in chromatin structure and function. Mitochondrial DNA mutations and their consequences in terms of human disease and aging. Novel ways to generate mutations and epimutations in cell lines and animal models.
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