Tmem200a, a transmembrane protein, has been associated with multiple biological processes and diseases. It may play a role in the regulation of adipose morphology, as functional evaluation by siRNA-mediated knockdown in adipose-derived precursor cells identified it as one of six genes controlling adipocyte renewal and differentiation [4]. Additionally, it has been implicated in the genomic instability-related gene signature for predicting the prognosis of acute myeloid leukemia patients [5].

In gastric cancer, studies have shown significant findings. Knockdown of Tmem200a in gastric cancer cells inhibited cell proliferation, decreased vimentin, N-cadherin, and Snai proteins, and inhibited AKT phosphorylation, suggesting its involvement in the PI3K/AKT signaling pathway and epithelial-mesenchymal transition (EMT) [1]. High expression of Tmem200a in gastric cancer tissues was associated with a poor prognosis, and it may be an independent risk factor for overall survival. It also showed a correlation with immune cell infiltration and immune checkpoint expression [3]. Meta-analysis and RT-qPCR validated its up-regulation in gastric cancer tissues compared to adjacent non-tumor tissues, and gene set enrichment analysis identified immune-related and tumor-related signaling pathways enriched in the high Tmem200A expression phenotype pathway [2].

In conclusion, Tmem200a is involved in diverse biological functions, especially in adipose development and disease prognosis. In gastric cancer, its role in cell proliferation, EMT, and immune infiltration, as revealed through in vitro loss-of-function studies, highlights its potential as a biomarker and therapeutic target. These findings contribute to a better understanding of the biological mechanisms underlying gastric cancer and other related diseases.