ArticleCancer cell international2020
Upregulation of ARHGAP30 attenuates pancreatic cancer progression by inactivating the β-catenin pathway.
Article in Cancer cell international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 15 papers.
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15 citing papers in PubMed, 23 citations in OpenAlex.
- Immune Infiltration Landscape in Osteosarcoma: Clinical Implications for Prognosis and Therapy.Cancer reports (Hoboken, N.J.) · 2026Article
- Loss of Arhgap39 facilitates cell migration and invasion in murine hepatocellular cancer cells.Oncology research · 2025Article
- A novel ARHGAP family gene signature for survival prediction in glioma patients.Journal of cellular and molecular medicine · 2024Article
- Whole-genome screens reveal regulators of differentiation state and context-dependent migration in human neutrophils.Nature communications · 2023Article
- PABPC1 promotes cell proliferation and metastasis in pancreatic adenocarcinoma by regulating COL12A1 expression.Immunity, inflammation and disease · 2023Article
- Knockdown of ARHGAP30 inhibits ovarian cancer cell proliferation, migration, and invasiveness by suppressing the PI3K/AKT/mTOR signaling pathway.European journal of histochemistry : EJH · 2023Article
- Fixing the GAP: The role of RhoGAPs in cancer.European journal of cell biology · 2022Review
- Identification of Tumor Antigens and Immune Subtypes of Glioblastoma for mRNA Vaccine Development.Frontiers in immunology · 2022Article
- Hyper-Methylated Hub Genes of T-Cell Receptor Signaling Predict a Poor Clinical Outcome in Lung Adenocarcinoma.Journal of oncology · 2022Article
- DNA methylation ofAging · 2021Article
- Overexpression of ARHGAP30 suppresses growth of cervical cancer cells by downregulating ribosome biogenesis.Cancer science · 2021Article
- ARHGAP10 inhibits the epithelial-mesenchymal transition of non-small cell lung cancer by inactivating PI3K/Akt/GSK3β signaling pathway.Cancer cell international · 2021Article
- The role of ARHGAP9: clinical implication and potential function in acute myeloid leukemia.Journal of translational medicine · 2021Article
- Trefoil Factor 2 Regulates Proliferation and Apoptosis of Pancreatic Cancer Cells and LPS-Induced Normal Pancreatic Duct Cells by β-Catenin Pathway.Cancer management and research · 2020Article
- Knockdown of 91 H Suppresses the Tumorigenesis of Osteosarcoma via Inducing Methylation of CDK4 Promoter.Technology in cancer research & treatmentArticle
Corrections and comments
- Retracted
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPancreatic cancer is a highly malignant gastrointestinal cancer that can widely metastasize during the early stage of disease, and it is associated with one of the worst prognoses among cancers. In this study, we aimed to investigate the function of Rho GTPase-activating protein 30 (ARHGAP30) in pancreatic cancer cells and thus propose a novel therapy for pancreatic cancer.
methodsARHGAP30 expression in tumor tissues from patients with pancreatic cancer as well as cell lines was detected using immunohistochemistry (IHC), real-time polymerase chain reaction, and western blotting. Cell proliferation, transwell, and apoptosis assays were performed and the levels of related proteins were determined after ARHGAP30 knockdown or overexpression. Additionally, in vivo experiments were performed on nude mice.
resultsARHGAP30 expression was found to be significantly increased in tumor tissues from patients with pancreatic cancer as well as in pancreatic cancer cell lines. IHC and prognostic analyses indicated that patients with high ARHGAP30 expression had a good prognosis. ARHGAP30 overexpression significantly decreased pancreatic cancer cell proliferation and metastasis; promoted apoptosis; reduced β-catenin, B-cell lymphoma 2 (Bcl-2), matrix metalloproteinase-2 (MMP2), and MMP9 expression; and increased Bcl-2-associated X protein (Bax) and cleaved caspase-3 expression. ARHGAP30 knockdown elicited the opposite effects. The effects of ARHGAP30 knockdown were potently attenuated by the β-catenin inhibitor XAV939. ARHGAP30 knockdown-induced RHOA activity was potently attenuated by the RHOA inhibitor CCG1423. In vivo, ARHGAP30 overexpression significantly inhibited lung metastasis in nude mice and increased the survival of mice with lung metastases.
conclusionsOur findings indicate that ARHGAP30 may function as a tumor suppressor in pancreatic cancer progression by regulating the expression of related genes and the β-catenin pathway.
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