Introduction: 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. Methods: 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. Results: 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. Conclusion: 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.

Introduction: In light of the increased demand for reliable cancer-associated biomarkers and ANLN oncogenic potential, the present study aimed to investigate ANLN’s role in 24 human cancers. Methods: The UALCAN, Kaplan–Meier (KM) plotter, TNM Plot, GENT2, GEPIA, HPA, cBioPortal, STRING, Enrichr, TIMER, Cytoscape, DAVID, MuTarget, and CTD online databases and bioinformatic tools were used in this study. Results: In three of the cancers analyzed, ANLN expression was downregulated in tumor tissue, while it was overexpressed in the 21 other types of tumor tissue relative to controls. In CESC, ESCA, HNSC, and KIRC patients, ANLN overexpression was correlated with shorter overall survival, relapse-free survival, and metastasis. This suggests that ANLN is significantly involved in the development and progression of these four cancers. Further expression analysis revealed upregulation of ANLN in CESC, ESCA, HNSC, and KIRC patients with different clinical characteristics, regardless of the heterogeneity barrier. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis revealed that ANLN-associated genes were coexpressed with ANLN and were included in diverse BP, MF, and KEGG terms. Moreover, some interesting correlations were also documented between ANLN expression and its promoter-methylation level, genetic alterations, other mutant genes, and CD8⁺ T- and CD4⁺ T-cell infiltration. Moreover, we also identified ANLN-associated transcription factors, miRNAs, and chemotherapeutic drugs. Conclusion: This pan-cancer study revealed the novel diagnostic and prognostic role of ANLN across four cancers, regardless of heterogeneity.