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Introduction: Transformer (TRA2B) is a serine/arginine-rich (SR)-like protein family that regulates the alternative splicing of several genes in a concentration-dependent manner. Amplification of the TRA2B gene, which codes for TRA2B, occurs in several malignancies, including those of the lung, cervix, head and neck, ovary, stomach, and uterine. Materials and methods: The present study design follows a computational approach to predict the molecular mechanisms underlying TRA2B alterations in two cancer phenotypes, viz., lung and head and neck squamous cell carcinoma. The genetic alteration in the TRA2B gene was identified using the cBioportal database. The gene expression pattern in both the cancer types and their survival pattern concerning the expression profile was demonstrated using UALCAN. The microRNA targets of the TRA2B gene were identified using the miRDB database. Results: Genetic alteration was found to be 27% and 48% in HNSCC and LUSC datasets, respectively. The alterations included gene amplification, missense, nonsense, and splice site mutations. The gene expression profile of TRA2B correlated well with the gene amplification demonstrated by patients in both groups. However, the upregulation of TRA2B did not correlate well with the survival profile in LUSC patients. The downregulation of TRA2B markedly affected the survival of HNSCC patients, which can be attributed to the functions of microRNAs targeting TRA2B transcripts. Conclusion: Although TRA2B was found to be a potential diagnostic marker exhibiting a differential expression pattern for HNSCC, the employability of this gene as a prognostic marker needs more experimentation. Also, the influence of microRNAs on dysregulated gene expression should be considered to gain a better understanding of the underlying molecular mechanisms precipitating the disease. |
