Multi-Omics Analysis Identified TMED2 as a Shared Potential Biomarker in Six Subtypes of Human Cancer

• Published in: International journal of general medicine Vol. 14; pp. 7025 - 7042
• Main Authors: Sial, Nuzhat, Saeed, Saba, Ahmad, Mukhtiar, Hameed, Yasir, Rehman, Abdul, Abbas, Mustansar, Asif, Rizwan, Ahmed, Hamad, Hussain, Muhammad Safdar, Rehman, Jalil Ur, Atif, Muhammad, Khan, Muhammad Rashid
• Format: Journal Article
• Language: English
• Published: New Zealand Dove Medical Press Limited 01-01-2021; Taylor & Francis Ltd; Dove; Dove Medical Press
• Subjects: biomarker; Biomarkers; Cancer; Cancer therapies; Datasets; Development and progression; Drug interactions; Esophagus; expression variations; Gene expression; Genes; Genetic engineering; Liver cancer; Medical prognosis; Methylation; Online databases; Original Research; Proteins; Software; tmed2; Pakistan; TMED2; cancer; expression variations; biomarker
• ISSN: 1178-7074; 1178-7074
• DOI: 10.2147/IJGM.S327367

Cancer is one of the most common malignancies and the leading cause of death worldwide. As a member of the transmembrane emp24 domain (Tmed)/p24 family of proteins, TMED2 expression variations have been documented earlier in only a few subtypes of human cancers, and the multi-omics profiling of TMED2 as a shared biomarker in different other subtypes of human cancers remains to be uncovered.
In the current study, TMED2 multi-omics analysis in 24 major subtypes of human cancer was performed using different authentic online databases and bioinformatics analysis including UALCAN, Kaplan-Meier (KM) plotter, Human Protein Atlas (HPA), GENT2, MEXPRESS, cBioportal, STRING, DAVID, TIMER, and CTD.
In general, the TMED2 expression in 24 major subtypes of human cancers was higher relative to normal controls and was also strongly associated with the lower overall survival (OS) and relapse-free survival (RFS) duration of CESC, ESCA, HNSC, KIRC, LIHC, and LUAD patients. This implies that TMED2 plays a significant role in the development and progression of these cancers. Furthermore, the TMED2 overexpression was also correlated with different clinicopathological features of CESC, ESCA, HNSC, KIRC, LIHC, and LUAD patients. TMED2-associated genes network was involved in 3 diverse pathways, and finally, few stronger correlations were also explored between TMED2 expression and its promoter methylation level, genetic alterations, and CD8+ T immune cells level.
In conclusion, via this in silico study, we have elucidated that TMED2 can serve as a shared diagnostic and prognostic biomarker in CESC, ESCA, HNSC, KIRC, LIHC, and LUAD patients of different clinicopathological features but, further in vitro and in vivo research should be carried out to confirm these findings.