ArticleJournal of translational medicine2018
GAP43, a novel metastasis promoter in non-small cell lung cancer.
Article in Journal of translational medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- The GAP43/RAC1 axis drives glycolytic reprogramming and progression in lung adenocarcinoma.Respiratory research · 2026Article
- Animal models of lung cancer: Phenotypic comparison of different animal models of lung cancer and their application in the study of mechanisms.Animal models and experimental medicine · 2025Review
- Clinically relevant stratification of lung squamous carcinoma patients based on ubiquitinated proteasome genes for 3P medical approach.The EPMA journal · 2024Article
- Identification and validation of a novel stress granules-related prognostic model in colorectal cancer.Frontiers in genetics · 2023Article
- Identification of Key Genes Associated with Brain Metastasis from Breast Cancer: A Bioinformatics Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2022Article
- Investigation of the Molecular Profile of Granular Cell Tumours and Schwannomas of the Oral Cavity.Dentistry journal · 2022Article
- Article
- lncRNA LOC100911717-targeting GAP43-mediated sympathetic remodeling after myocardial infarction in rats.Frontiers in cardiovascular medicine · 2022Article
- TGF-β promote epithelial-mesenchymal transition via NF-κB/NOX4/ROS signal pathway in lung cancer cells.Molecular biology reports · 2021Article
- The association of CMTM6 expression with prognosis and PD-L1 expression in triple-negative breast cancer.Annals of translational medicine · 2021Article
- Proteomic Analysis of Rhesus Macaque Brain Explants Treated WithFrontiers in cellular and infection microbiology · 2021Article
- Thermosensitive heparin-poloxamer hydrogel encapsulated bFGF and NGF to treat spinal cord injury.Journal of cellular and molecular medicine · 2020Article
- Non-disruptive mutation inAnnals of translational medicine · 2020Article
- Growth-associated protein 43 promotes thyroid cancer cell lines progression via epithelial-mesenchymal transition.Journal of cellular and molecular medicine · 2019Article
- Ubiquitin specific peptidase 49 inhibits non-small cell lung cancer cell growth by suppressing PI3K/AKT signaling.The Kaohsiung journal of medical sciences · 2019Article
- A common signature of brain metastases among patients with breast cancer, melanoma, and lymphoma.Neuro-oncology advancesArticle
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundBrain metastasis is an extremely serious sequela with a dismal prognosis in non-small cell lung cancer (NSCLC). The present study aimed to identify novel biomarkers and potential therapeutic targets for brain metastases of NSCLC.
methodsWe performed high-throughput Luminex assays to profile the transcriptional levels of 36 genes in 70 operable NSCLC patients, among whom 37 developed brain metastases as the first relapse within 3 years after surgery. The Cox proportional hazards regression model was used to evaluate the association between genes and brain metastases. Wound healing assay and transwell assay was carried out to estimate the function of target gene in vitro. And left ventricular injection on nude mice was used to evaluate the effect of target gene in vivo.
resultsGrowth-associated protein 43 (GAP43) was found to be related to brain metastasis. Multivariate Cox regression analysis showed that NSCLC patients with elevated GAP43 had a 3.29-fold increase in the risk for brain metastasis compared with those with low levels (95% confidence interval: 1.55-7.00; P = 0.002). Kaplan-Meier survival curves revealed that GAP43 was also associated with overall survival. Analysis of a cohort of 1926 NSCLC patients showed similar results: patients with high levels of GAP43 had worse progression-free and overall survival rates. Furthermore, in vitro experiments showed that GAP43 facilitated cell migration. Animal studies demonstrated that GAP43-silenced NSCLC cells were less likely to metastasize to the brain and bone than control cells. Immunofluorescence and F-actin/G-actin in vivo assays indicated that GAP43 knockdown triggered depolymerization of the F-actin cytoskeleton. Rho GTPase activation assays showed that Rac1 was deactivated after GAP43 was silenced.
conclusionsOur findings suggest that GAP43 is an independent predictor of NSCLC brain metastasis and that it may facilitate metastasis by regulating the Rac1/F-actin pathway.
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