Qsox1, or quiescin sulfhydryl oxidase 1, is an enzyme that oxidizes thiols during protein folding, reducing molecular oxygen to hydrogen peroxide [6]. It is involved in multiple biological pathways. For instance, it has a role in disulfide bond formation in proteins and can influence redox homeostasis. Its functions are crucial in various biological processes, and its dysregulation is associated with several diseases [6]. Genetic models, such as knockout mouse models, are valuable for studying its functions.

In NSCLC, aberrant RNA m5C hypermethylation via the NSUN2-YBX1-QSOX1 axis mediates intrinsic resistance to gefitinib. NSUN2 methylates the QSOX1 coding sequence region, enhancing its translation through YBX1 [1]. In esophageal cancer, QSOX1 in dormant cancer stem cells promotes PD-L1 upregulation and CD8 T cell exclusion, facilitating immune escape, and its inhibition combined with immunotherapy and chemotherapy may prevent recurrence [2]. In the colon, QSOX1 knockout mice have impaired mucus barrier function due to sialylation defects in gut mucus, showing that QSOX1 redox control of sialylation is essential for mucosal function [3]. In preeclampsia, QSOX1 is overexpressed in the placenta, and its knockdown in HTR-8/SVneo cells attenuates apoptosis and intracellular H2O2 levels, indicating hypoxia-induced QSOX1 contributes to apoptosis in PE placentae [4]. A molecular inhibitor of QSOX1, SBI-183, suppresses tumor growth in renal cell carcinoma xenograft mouse models, suggesting it could be a novel anticancer agent for QSOX1-overexpressing tumors [5].

In conclusion, Qsox1 is involved in a wide range of biological functions, including protein folding, redox regulation, and immune-related processes. Through gene knockout and inhibitor-based studies, its role in cancer drug resistance, immune escape, and maintaining mucosal function has been revealed. These findings provide insights into potential therapeutic strategies for diseases like cancer and preeclampsia.