ArticleOncoTargets and therapy2015
GIT1 is a novel prognostic biomarker and facilitates tumor progression via activating ERK/MMP9 signaling in hepatocellular carcinoma.
Article in OncoTargets and therapy, 2015. 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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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- The Discovery of GIT1/β-Pix Inhibitors: Virtual Screening and Biological Evaluation of New Small-molecule Compounds with Anti-invasion Effect in Gastrointestinal Neoplasms.Drug design, development and therapy · 2024Article
- Proteomic Markers for Mechanobiological Properties of Metastatic Cancer Cells.International journal of molecular sciences · 2023Review
- G-Protein-Coupled Receptor Kinase-Interacting Protein 1 (GIT1) Promotes Head and Neck Squamous Cell Carcinoma Metastases via Activating the PI3K/AKT/mTOR Signal Pathway.Computational and mathematical methods in medicine · 2022Article
- Article
- FOXP3 promotes colorectal carcinoma liver metastases by evaluating MMP9 expression via regulating S-adenosylmethionine metabolism.Annals of translational medicine · 2020Article
- The Arf-GAP and protein scaffold Cat1/Git1 as a multifaceted regulator of cancer progression.Small GTPases · 2020Review
- Quercetin Inhibits the Migration and Invasion of HCCLM3 Cells by Suppressing the Expression of p-Akt1, Matrix Metalloproteinase (MMP) MMP-2, and MMP-9.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Inhibiting GIT1 reduces the growth, invasion, and angiogenesis of osteosarcoma.Cancer management and research · 2018Article
- Snail collaborates with EGR-1 and SP-1 to directly activate transcription of MMP 9 and ZEB1.Scientific reports · 2017Article
- GIT1 gene deletion delays chondrocyte differentiation and healing of tibial plateau fracture through suppressing proliferation and apoptosis of chondrocyte.BMC musculoskeletal disorders · 2017Article
- Arf proteins in cancer cell migration.Small GTPases · 2016Review
- Expanding functions of GIT Arf GTPase-activating proteins, PIX Rho guanine nucleotide exchange factors and GIT-PIX complexes.Journal of cell science · 2016Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimMultiple studies have revealed that G-protein-coupled receptor kinase-interacting protein 1 (GIT1) is overexpressed in many cancers and facilitates tumor progression. However, the role of GIT1 in hepatocellular carcinoma (HCC) remains unclear.
methodsGIT1 expression was detected in cell lines and 130 pairs of HCC and matched adjacent noncancerous samples. Transwell assay, flow cytometry, caspase 3/7 activity assay, 5-bromodeoxyuridine cell proliferation assay, and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay were used to assess invasion, migration, apoptosis, and proliferation of HCC cells. Furthermore, GIT1 expression was detected by immunohistochemistry to evaluate its correlation with phospho-extracellular signal-regulated kinase (p-ERK)1/2. The regulatory effect of GIT1 on ERK1/2, p-ERK1/2, and matrix metalloproteinase-9 (MMP9) in HCC cells was confirmed by immunoblotting.
resultsIn this study, we demonstrated that GIT1 was more highly expressed in HCC samples than that in non-HCC samples, and overexpression of GIT1 was correlated with clinicopathological features of poor prognosis. Clinical analysis demonstrated that GIT1 is an independent prognostic biomarker for predicting overall survival and disease-free survival of patients with HCC. In vitro studies showed that downregulation of GIT1 facilitated HCC cell apoptosis and repressed HCC cell invasion, migration, and proliferation. Overexpression of GIT1 is associated with p-ERK1/2 amplification in HCC tissues. Moreover, downregulation of GIT1 resulted in inactivation of ERK signaling and downregulation of MMP9.
conclusionOur findings indicate that GIT1 is an independent prognostic biomarker and facilitates HCC progression via activating ERK/MMP9 signaling.
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