Osbpl3, or oxysterol-binding protein like protein 3, is a member of the oxysterol-binding protein superfamily and functions as an intracellular lipid receptor. It is involved in some pathological and physiological processes during tumor progression, and may be associated with signaling pathways such as RAS and R-Ras/Akt [2,4].

In colorectal cancer (CRC), Osbpl3 is significantly overexpressed in tumor tissues, associated with worse progression-free and overall survival, and negatively correlated with tumor differentiation. KRAS mutations are significantly associated with high Osbpl3 expression, and Osbpl3 and Ki-67 expression are also significantly correlated. Additionally, over-expression of Osbpl3 promotes CRC cell proliferation, invasion, and metastasis both in vitro and in vivo through activation of the RAS signaling pathway, and HIF-1A can up-regulate Osbpl3 by binding to its promoter [1,2].

In pancreatic cancer, high Osbpl3 expression is associated with immunosuppressive characteristics like reduced CD8+ T cell infiltration and increased Treg cells and M2 macrophages, and is linked to resistance to immunotherapy [3].

In gastric cancer, knockdown of Osbpl3 reduces cell growth in vitro and in vivo by inhibiting cell cycle progression, as it activates the R-Ras/Akt signaling pathway [4].

In conclusion, Osbpl3 plays a crucial role in the development and progression of multiple cancers including CRC, pancreatic cancer, and gastric cancer. Studies on Osbpl3, especially through loss-of-function experiments in relevant models, help to understand its role in tumor-related biological processes, providing potential therapeutic targets for these diseases.