ArticleExperimental and therapeutic medicine2023
Forkhead box protein K1‑regulated neurexophilin 4 promotes proliferation, metastasis and glycolysis in colorectal cancer.
Article in Experimental and therapeutic medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 2 citations in OpenAlex.
- Neurexophilin 4 facilitates the malignant progression of kidney renal clear cell carcinoma by regulating PI3K/AKT-mediated glycolysis.Molecular genetics and genomics : MGG · 2026Article
- High expression of NXPH4 correlates with poor prognosis, metabolic reprogramming, and immune infiltration in colon adenocarcinoma.Journal of gastrointestinal oncology · 2024Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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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Registered trials
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