GOLM1, also known as GP73 or GOLPH2, is a Golgi - resident type 2 transmembrane protein. It has been associated with multiple biological processes, such as lipid metabolism, cytokine production, and regulation of various signaling pathways. Its overexpression is observed in several cancers and some infectious diseases, indicating its significance in disease - related biological functions [3,7].

In HCC, GOLM1 promotes CD8+ T cell suppression by enhancing exosomal PD - L1 transport into tumor - associated macrophages, highlighting its role in shaping the immunosuppressive microenvironment [1]. In pulmonary fibrosis, GOLM1 - knockout mice showed alleviated fibrosis and collagen deposition, suggesting that GOLM1 promotes pulmonary fibrosis through the GOLM1 - KLF4 - NEAT1 signaling axis [2]. In prostate cancer, GOLM1 interacts with PSMD1 to enhance AR - driven transcriptional activation and promote cancer progression. It also promotes epithelial - mesenchymal transition (EMT) by activating the TGFβ1/Smad2 signaling pathway [4,6]. In atherosclerosis, global deletion of GOLM1 in Apoe - / - mice ameliorated inflammation and atherosclerosis, as extracellular GOLM1 activates macrophage EGFR - ERK signaling cascade [5]. In colorectal cancer, overexpression of GOLM1 promotes immune escape and metastasis by recruiting myeloid - derived suppressor cells (MDSCs) [8].

In conclusion, GOLM1 plays crucial roles in multiple diseases, including cancer, pulmonary fibrosis, and atherosclerosis. Gene - knockout mouse models have been instrumental in revealing these functions, providing potential therapeutic targets for these disease areas. Its functions range from regulating the immune microenvironment, promoting fibrosis, enhancing cancer - associated signaling pathways, to driving atherogenesis.