Forkhead box protein K1-regulated neurexophilin 4 promotes proliferation, metastasis and glycolysis in colorectal cancer

被引:3
|
作者
Fan, Qiulin [1 ]
He, Wan [2 ]
Shang, Yuanjiang [3 ,4 ]
机构
[1] Shanghai Tenth Peoples Hosp, Ctr Reprod Med, Shanghai 200072, Peoples R China
[2] Shanghai Tenth Peoples Hosp, Dept Blood Transfus, Shanghai 200072, Peoples R China
[3] Shanghai Tenth Peoples Hosp, Clin Lab, Shanghai 200072, Peoples R China
[4] Shanghai Tenth Peoples Hosp, Clin Lab, 301 Yanchang Middle Rd, Shanghai 200072, Peoples R China
关键词
neurexophilin; 4; forkhead box protein K1; proliferation; metastasis; glycolysis; colorectal cancer;
D O I
10.3892/etm.2023.12133
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
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.
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页数:10
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