ArticleMolecular and cellular biochemistry2013
Small interfering RNA targeting Rac1 sensitizes colon cancer to dihydroartemisinin-induced cell cycle arrest and inhibited cell migration by suppressing NFκB activity.
Article in Molecular and cellular biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Unraveling tissue-specific molecular targets of dihydroartemisinin in non-small cell lung cancer: an integrative machine learning and network pharmacology approach.Medical oncology (Northwood, London, England) · 2025Article
- Rac1 in gastric cancer: a molecular driver of invasion, EMT, and therapeutic resistance.Journal of translational medicine · 2025Review
- Dihydroartemisinin: A Potential Natural Anticancer Drug.International journal of biological sciences · 2021Review
- Rac-GEF/Rac Signaling and Metastatic Dissemination in Lung Cancer.Frontiers in cell and developmental biology · 2020Article
- Antitumor Research on Artemisinin and Its Bioactive Derivatives.Natural products and bioprospecting · 2018Review
- Effect of dihydroarteminin combined with siRNA targeting Notch1 on Notch1/c-Myc signaling in T-cell lymphoma cells.Experimental and therapeutic medicine · 2018Article
- PRPF overexpression induces drug resistance through actin cytoskeleton rearrangement and epithelial-mesenchymal transition.Oncotarget · 2017Article
- Repurposing the anti-malarial drug dihydroartemisinin suppresses metastasis of non-small-cell lung cancer via inhibiting NF-κB/GLUT1 axis.Oncotarget · 2016Article
- p104 binds to Rac1 and reduces its activity during myotube differentiation of C2C12 cell.TheScientificWorldJournal · 2014Article
- Small Interfering RNA in Colorectal Cancer Liver Metastasis Therapy.Technology in cancer research & treatmentArticle
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dihydroartemisinin (DHA) has recently shown antitumor activity in various cancer cells. The small GTPase Rac1 regulates many cellular processes, including cytoskeletal reorganization, cell migration, proliferation, and survival. In addition, Rac1 plays a major role in activating NFκB-mediated transcription. Both Rac1 and NFκB regulate many properties of the malignant phenotype, including anchorage-independent proliferation and survival, metastasis, and angiogenesis. In this study, for the first time, we demonstrated that Rac1 knockdown can enhance DHA-induced growth inhibition, cell cycle arrest, apoptosis, and migration in both HCT116 and RKO cell lines in vitro. The mechanism is due partially to DHA, and Rac1 siRNA deactivates NFκB activity, so as to decrease tremendously the expression of its target gene products, such as PCNA, cyclin D1, and CDK4; and increase the expression of p21, cleaved-caspase-3, and cleaved-PARP. In our in vivo studies, DHA also manifested remarkably enhanced antitumor effect when combined with Rac1 siRNA. We concluded that inhibition of NFκB activation is one of the mechanisms that Rac1 siRNA dramatically promotes DHAs antitumor effect on human colon cancer.
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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.