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SELPLG, also known as selectin P ligand gene, encodes P-selectin glycoprotein ligand 1 (PSGL-1). PSGL-1 is involved in the receptor/ligand complex with P-selectin, playing key roles in inflammatory response, atherosclerotic process, and cell migration. It is also associated with lymphocyte recruitment, which is critical in the pathogenesis of certain diseases [3,4,5].

In osteosarcoma, lnc-SELPLG-2:1 (a long non-coding RNA related to SELPLG) acts as an oncogenesis activator. Inhibition of lnc-SELPLG-2:1 accelerates cell apoptosis and suppresses cell proliferation, migration, and invasion, while its overexpression has the opposite effects. The mechanism involves the hsa-miR-10a-5p/BTRC cascade, where lnc-SELPLG-2:1 competitively binds to hsa-miR-10a-5p, preventing BTRC from miRNA-mediated degradation, thus promoting osteosarcoma cell progression [1].

In acute respiratory distress syndrome (ARDS), SELPLG lung tissue expression increases in mice exposed to lipopolysaccharide (LPS)-and ventilator-induced lung injury. A recombinant tandem PSGL1 immunoglobulin fusion molecule can decrease SELPLG lung tissue expression and protect from lung injury. SELPLG promoter activity is regulated by hypoxia-inducible transcription factors and NRF2, and DNA methylation also affects its expression [2].

In conclusion, SELPLG is crucial in multiple biological processes and disease conditions. Its role in osteosarcoma oncogenesis and in ARDS pathogenesis has been revealed through in-vitro and in-vivo studies. Understanding SELPLG may provide insights into disease mechanisms and potential therapeutic targets for these diseases.