TMEM132A has recently been identified as a potential contributor to tumorigenesis. Nevertheless, a thorough examination of TMEM132A in human tumors across various cancer types has not been conducted to date. The expression of TMEM132A was analyzed in 33 different types of human tumors by utilizing data from the TCGA and GTEx databases. TMEM132A was found to be significantly increased in 27 different types of cancer. High TMEM132A expression was linked to worse overall survival in KIRC, MESO, SARC and UVM, as well as unfavorable disease-free survival in KIRC and PRAD. The S530 locus of TMEM132A had lower phosphorylation in GBM but higher in HNSC, PAAD, LUAD and LUSC tumors. The S914 locus had higher phosphorylation in HNSC, KIRC, PAAD and LUSC tumors. TMEM132A genetic changes were thoroughly studied in different types of tumors using TCGA data. SKCM had the highest TMEM132A alteration frequency at 6.53%, predominantly characterized by “Mutation.” TMEM132A was significantly correlated with m1A, m5C and m6A genes in STAD, UCEC, GBM and DLBC tumors. TMEM132A was also associated with CAFs in various TCGA tumors. TMEM132A was positively correlated with immune genes in most cancers, but negatively correlated in CHOL and LIHC. We found a strong correlation between TMEM132A and TMB, MSI and HRD in various types of cancer. TMEM132A was positively correlated with APBA2, B4GALNT4, CDK5, CLSTN1 and PRPF19 genes. The heatmap confirms this correlation across different tumors. An analysis of the overlap between these groups identified ENOPH1 as a shared member. Finaly, GO enrichment and KEGG pathway were used to understand the functional role of TMEM132A in tumor development. GO enrichment highlighted terms like “endomembrane system” and “nervous system development” as important for TMEM132A’s impact. KEGG pathway analysis identified pathways such as “Axon guidance” and “Wnt signaling pathway” as relevant to TMEM132A’s influence on tumor pathogenesis. This is the first pan-cancer study to deeply understand the role of TMEM132A in tumor development across various types of cancers.
Chu et al. (Sun,) studied this question.