ArticleInternational journal of clinical and experimental pathology2017
ARHGAP9 siRNA inhibits gastric cancer cell proliferation and EMT via inactivating Akt, p38 signaling and inhibiting MMP2 and MMP9.
Article in International journal of clinical and experimental pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The trial behind it
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Who cites it
8 citing papers in PubMed.
- Effect of ARHGAP9 on Chemoresistance in High-Risk Advanced Retinoblastoma via the Rac1/β-Catenin/LEF1 Signaling Axis.Investigative ophthalmology & visual science · 2026Article
- Specific effects of hypoxia-immune core geneTranslational cancer research · 2025Article
- siRNA-based strategies to combat drug resistance in gastric cancer.Medical oncology (Northwood, London, England) · 2024Review
- ARHGAP6 inhibits bladder cancer cell viability, migration, and invasion via β-catenin signaling and enhances mitomycin C sensitivity.Human cell · 2023Article
- Effect of Rho GTPase activating protein 9 combined with preoperative ratio of platelet distribution width to platelet count on prognosis of patients with serous ovarian cancer.Translational cancer research · 2021Article
- The role of ARHGAP9: clinical implication and potential function in acute myeloid leukemia.Journal of translational medicine · 2021Article
- Different transcriptome profiles between human retinoblastoma Y79 cells and an etoposide-resistant subline reveal a chemoresistance mechanism.BMC ophthalmology · 2020Article
- ARHGAP9 suppresses the migration and invasion of hepatocellular carcinoma cells through up-regulating FOXJ2/E-cadherin.Cell death & disease · 2018Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveARHGAP9 is a RhoGTPase activating protein. This study aimed to investigate the effect of ARHGAP9 on cell proliferation of gastric cancer cell.
methodsHuman gastric cancer cell line SGC7901 were transfected with ARHGAP9 siRNA and the expression of epithelial to mesenchymal transition (EMT) factors, MMPs, and activated status of Akt and p38 signaling were detected. Moreover, the migration, invasion, and viability of SGC7901 cells were determined.
resultsARHGAP9 siRNA successfully inhibited cell viability, migration and invasion. The expression of E-cadherin was significantly upregulated, and expression of Snail, Vimentin, as well as MMP2 and MMP9 were obviously downregulated. Moreover, ARHGAP9 siRNA promoted inactivation of Akt and p38 signaling by inhibiting expression of p-Akt and p-p38.
conclusionThis study showed that ARHGAP9 contributed to the viability, migration, invasion as well as EMT in gastric cancer cell line SGC7901. ARHGAP9 might be used as a therapeutic target for gastric cancer.
Indexed as
Identifiers
31966562PMC6966049What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.