结直肠癌（CRC）是一种常见的恶性肿瘤。目前，对CRC在分子和基因水平上形成、发展和治疗的深入研究是一个研究热点。去神经元粘黏素4（NXPH4）的表达在多种癌症中已被发现异常增高，但其在CRC中的表达尚未报道。首先，使用相关数据库预测NXPH4在CRC中的表达以及与CRC患者生存率的关联。随后，通过细胞实验验证了CRC细胞中NXPH4的表达。使用细胞计数试剂盒-8、5-乙炔基-2'-脱氧尿嘧啶染色、流式细胞术、划痕愈合实验、Transwell实验、Western blotting和试剂盒检测了NXPH4在CRC细胞中的敲低对细胞增殖、侵袭、迁移和糖酵解的影响。使用JASPAR数据库预测了NXPH4和转录因子FOXK1之间的关联，并通过荧光素酶报告基因和染色质免疫沉淀实验证实了这种关联。还讨论了NXPH4的调节机制。结果显示，在CRC中NXPH4高度表达。CRC细胞中的NXPH4敲低可以显著抑制细胞增殖并诱导凋亡。NXPH4敲低抑制了细胞的侵袭、迁移和糖酵解。进一步，在CRC细胞中过表达FOXK1可以逆转上述过程。总之，FOXK1调控的NXPH4在CRC中促进了增殖、转移和糖酵解。版权所有：Fan等。

Colorectal cancer (CRC) is a common malignant tumor. At present, the in-depth study of the formation, development and treatment of CRC at the molecular and gene levels is a research hot spot. Neurexophilin 4 (NXPH4) expression has been revealed to be abnormally elevated in several types of cancer, but its expression in CRC has not yet been reported. First, relevant databases were used to predict the expression of NXPH4 in CRC and its association with the survival rate of patients with CRC. Subsequently, the expression of NXPH4 in CRC cells was verified through cell experiments. Cell Counting Kit-8, 5-ethynyl-2'-deoxyuridine staining, flow cytometry, wound healing assay, Transwell assay, western blotting and the kits were used to detect the effects of NXPH4 knockdown in CRC cells on cell proliferation, invasion, migration and glycolysis. The association between NXPH4 and forkhead box protein K1 (FOXK1) was predicted using the JASPAR database, and verified through luciferase reporter gene and chromatin immunoprecipitation experiments. The NXPH4 regulation mechanism was also discussed. NXPH4 was revealed to be highly expressed in CRC. NXPH4 knockdown in CRC cells could significantly inhibit cell proliferation and induce apoptosis. NXPH4 knockdown inhibited cell invasion, migration and glycolysis. The aforementioned process could be reversed by further FOXK1 overexpression in CRC cells. In conclusion, FOXK1-regulated NXPH4 promotes proliferation, metastasis and glycolysis in CRC.Copyright: © Fan et al.