ArticleJournal of cellular and molecular medicine2022
Nucleobindin-2/nesfatin-1 enhances the cell proliferation, migration, invasion and epithelial-mesenchymal transition in gastric carcinoma.
Article in Journal of cellular and molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 15 citations in OpenAlex.
- The role and mechanism by which micropeptide WHPP promote refractory wound healing.Journal of translational medicine · 2026Article
- Variants in the neuropeptide geneAmerican journal of cancer research · 2025Article
- Differential effects of nesfatin-1 on proliferation and migration in normal and cancerous human lung cells via the PI3K/AKT pathway.Animal cells and systems · 2025Article
- Salidroside inhibits melanin synthesis and melanoma growth via mTOR and PI3K/Akt pathways.Frontiers in oncology · 2025Article
- Research progress on the relationship between Nesfatin-1 and glucose metabolism.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Review
- Nucleobindin 2 inhibits senescence in gastric carcinoma.Scientific reports · 2024Article
- Plasma cell signatures predict prognosis and treatment efficacy for lung adenocarcinoma.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- Bone marrow adipocytes and lung cancer bone metastasis: unraveling the role of adipokines in the tumor microenvironment.Frontiers in oncology · 2024Review
- A cross-sectional study on the Nesfatin-1 serum levels of Vietnamese patients with pre-diabetes.Revista da Associacao Medica Brasileira (1992) · 2023Article
- The role of the stemness index-associated signature in the analysis of the tumorigenesis of liver cancer patients of different races.American journal of cancer research · 2023Article
- Nucleobindin-2/nesfatin-1 enhances the cell proliferation, migration, invasion and epithelial-mesenchymal transition in gastric carcinoma.Journal of cellular and molecular medicine · 2022Article
- NUCB2/Nesfatin-1 Couples Cholesterol Biosynthesis to Keratinocyte Migration to Accelerate Re-Epithelialisation in Cutaneous Wound Repair.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair SocietyArticle
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nesfatin-1, a newly discovered adipokine derived from nucleobindin-2 (NUCB2), has been described as a new prognostic marker in cancers. This study aimed to explore the functional role of NUCB2/nesfatin-1 in the cell proliferation, migration and invasion in gastric carcinoma (GC). The expressions of NUCB2/nesfatin-1 in GC tissues and normal adjacent tissues (NATs) were compared, and the effect of inhibition of NUCB2/nesfatin-1 on the cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) in GC cell line SGC-7901 was investigated. Cell transfection was conducted to inhibit NUCB2/nesfatin-1 by short hairpin RNA. Cell proliferation, migration and invasion abilities were determined using cell counting kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EdU), wound healing and transwell assays, respectively. The expressions of EMT markers E-Cadherin and N-Cadherin were determined using western blotting. The expression of NUCB2/nesfatin-1 protein in GC tissues was significantly increased compared with that in NATs. Consistently, the serum concentrations of NUCB2/nesfatin-1 were significantly higher in patients with GC as compared with those in the control group. Moreover, the results of CCK-8 assay and EdU assay indicated that knockdown of NUCB2/nesfatin-1 could markedly decrease SGC-7901 proliferation. Furthermore, the results of wound healing assay and transwell assay demonstrated that knockdown of NUCB2/nesfatin-1 significantly suppressed SGC-7901 migration and invasion abilities. Additionally, knockdown of NUCB2/nesfatin-1 decreased the expressions of N-Cadherin and increased the expressions of E-Cadherin in SGC-7901 cells. These findings suggest that knockdown of NUCB2/nesfatin-1 suppressed the proliferation, migration, invasion and EMT of SGC-7901 cells, suggesting a potentially promising therapeutic target for GC.
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