ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2015
Involvement of NEDD9 in the invasion and migration of gastric cancer.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Expression of NEDD9 and connexin-43 in neoplastic and stromal cells of gastric adenocarcinoma.Bosnian journal of basic medical sciences · 2021Article
- Prognostic Significances of NEDD-9 and FOXL-1 Expression in Intestinal Type Gastric Carcinoma: an Immunohistochemical Study.Journal of gastrointestinal cancer · 2021Article
- Review
- NEDD9 promotes invasion and migration of colorectal cancer cell line HCT116 via JNK/EMT.Oncology letters · 2019Article
- NEDD9 Facilitates Hypoxia-Induced Gastric Cancer Cell Migration via MICAL1 Related Rac1 Activation.Frontiers in pharmacology · 2019Article
- Overexpression of NEDD9 in renal cell carcinoma is associated with tumor migration and invasion.Oncology letters · 2017Article
- MicroRNA-335-5p is a potential suppressor of metastasis and invasion in gastric cancer.Clinical epigenetics · 2017Article
- High expression of HEF1 predicts a poorer prognosis of hepatocellular carcinoma: A retrospective study.Molecular and clinical oncology · 2016Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies have demonstrated that neural precursor cell expressed, developmentally downregulated 9 (NEDD9) is highly expressed in various tumor tissues and cell lines. However, research on the role of NEDD9 in gastric cancer (GC) is rare, and the potential mechanism in tumor progression has not yet been explored. In this study, we investigated the role and mechanism of NEDD9 in GC. The expression of NEDD9 in GC tissues and cell lines was measured by immunohistochemistry, qRT-PCR, and Western blot, respectively. Inhibiting NEDD9 expression was carried out by siRNA transfection, and upregulating of NEDD9 was via NEDD9 overexpression plasmid. The ability of proliferation, migration, and invasion was detected by MTT assay, scratch wound assay, and transwell assay, respectively. The expression of vimentin, E-cadherin, Zeb1, and Zeb2 was measured by Western blot and qRT-PCR. We found that NEDD9 expression was dramatically increased both in GC tissues and cell lines, and the expression was significantly related to GC development. Knockdown of NEDD9 in SGC-7901 strongly inhibited its malignant capacity in vitro. Meanwhile, upregulation of NEDD9 in GES-1 increased the malignant capacity. In addition, the expression of vimentin, Zeb1, and Zeb2 was positively correlated with NEDD9, while E-cadherin was opposite. Collectively, our findings suggest that NEDD9 acts as an oncogene and promotes GC metastasis via EMT.
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