ArticleJournal of the National Cancer Institute2013
Synbindin in extracellular signal-regulated protein kinase spatial regulation and gastric cancer aggressiveness.
Article in Journal of the National Cancer Institute, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 58 citations in OpenAlex.
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- Acetylation increases expression, interaction with TRAPPC4 and surface localization of PD-L1.Discover oncology · 2023Article
- MCT4 Promotes Hepatocellular Carcinoma Progression by Upregulating TRAPPC5 Gene.Journal of hepatocellular carcinoma · 2022Article
- TRAPPC4 regulates the intracellular trafficking of PD-L1 and antitumor immunity.Nature communications · 2021Article
- mMolecular cancer · 2020Article
- KLF5 and MYC modulated LINC00346 contributes to gastric cancer progression through acting as a competing endogeous RNA and indicates poor outcome.Cell death and differentiation · 2019Article
- MicroRNA-1275 inhibits cell migration and invasion in gastric cancer by regulating vimentin and E-cadherin via JAZF1.BMC cancer · 2019Article
- Long noncoding RNA GAPLINC promotes gastric cancer cell proliferation by acting as a molecular sponge of miR-378 to modulate MAPK1 expression.OncoTargets and therapy · 2018Article
- Low expression of trafficking protein particle complex 4 predicts poor prognosis in hepatocellular carcinoma.International journal of clinical and experimental pathology · 2018Article
- CD133 mediates the TGF-β1-induced activation of the PI3K/ERK/P70S6K signaling pathway in gastric cancer cells.Oncology letters · 2017Article
- Scaffold Proteins in Gastrointestinal Tumors as a Shortcut to Oncoprotein Activation.Gastrointestinal tumors · 2017Review
- A novel long noncoding RNA-LOWEG is low expressed in gastric cancer and acts as a tumor suppressor by inhibiting cell invasion.Journal of cancer research and clinical oncology · 2016Article
- Upregulation of the Non-Coding RNA OTUB1-isoform 2 Contributes to Gastric Cancer Cell Proliferation and Invasion and Predicts Poor Gastric Cancer Prognosis.International journal of biological sciences · 2016Article
- Syndecans as Cell Surface Receptors in Cancer Biology. A Focus on their Interaction with PDZ Domain Proteins.Frontiers in pharmacology · 2016Review
- Treatment of cholestatic fibrosis by altering gene expression of Cthrc1: Implications for autoimmune and non-autoimmune liver disease.Journal of autoimmunity · 2015Article
- Antisense Long Noncoding RNA HIF1A-AS2 Is Upregulated in Gastric Cancer and Associated with Poor Prognosis.Digestive diseases and sciences · 2015Article
- Scaffold proteins in cancer.Oncoscience · 2015Article
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe molecular mechanisms that control the aggressiveness of gastric cancer (GC) remain poorly defined. Here we show that synbindin contributes to the aggressiveness of GC by activating extracellular signal-regulated protein kinase (ERK) signaling on the Golgi apparatus.
methodsExpression of synbindin was examined in normal gastric mucosa (n = 44), intestinal metaplastic gastric mucosa (n = 66), and GC tissues (n=52), and the biological effects of synbindin on tumor growth and ERK signaling were detected in cultured cells, nude mice, and human tissue samples. The interaction between synbindin and mitogen-activated protein kinase kinase (MEK1)/ERK was determined by immunofluorescence and fluorescence resonance energy transfer assays. The transactivation of synbindin by nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) was detected using luciferase reporter assay and chromatin immunoprecipitation.
resultsHigh expression of synbindin was associated with larger tumor size (120.8 vs 44.8 cm(3); P = .01), advanced tumor node metastasis (TNM) stage (P = .003), and shorter patient survival (hazard ratio = 1.51; 95% confidence interval [CI] = 1.01 to 2.27; P = .046). Synbindin promotes cell proliferation and invasion by activating ERK2 on the Golgi apparatus, and synbindin is directly transactivated by NF-κB. Synbindin expression level was statistically significantly higher in human GCs with activated ERK2 than those with low ERK2 activity (intensity score of 11.5, 95% CI = 10.4 to 12.4 vs intensity score of 4.6, 95% CI 3.9 to 5.3; P < .001). Targeting synbindin in xenograft tumors decreased ERK2 phosphorylation and statistically significantly reduced tumor volume (451.2mm(3), 95% CI = 328.3 to 574.1 vs 726.1mm(3), 95% CI = 544.2 to 908.2; P = .01).
conclusionsSynbindin contributes to malignant phenotypes of GC by activating ERK on the Golgi, and synbindin is a potential biomarker and therapeutic target for GC.
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