ArticleCancer gene therapy2011
Role of Rac1-dependent NADPH oxidase in the growth of pancreatic cancer.
Article in Cancer gene therapy, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 43 citations in OpenAlex.
- Differential Sensitivity to MEK Inhibitors Highlights Distinct Entosis Mechanisms in BxPC3 and MCF7 Cells.Cells · 2025Article
- Rac1 GTPase Regulates the βTrCP-Mediated Proteolysis of YAP Independently of the LATS1/2 Kinases.Cancers · 2024Article
- CYRI-B-mediated macropinocytosis drives metastasis via lysophosphatidic acid receptor uptake.eLife · 2024Article
- Nicotinamide adenine dinucleotide phosphate oxidase in pancreatic diseases: Mechanisms and future perspectives.World journal of gastroenterology · 2024Review
- The potential role of reprogrammed glucose metabolism: an emerging actionable codependent target in thyroid cancer.Journal of translational medicine · 2023Review
- Metabolic Adaptation-Mediated Cancer Survival and Progression in Oxidative Stress.Antioxidants (Basel, Switzerland) · 2022Review
- RhoGDI2 induced malignant phenotypes of pancreatic cancer cells via regulating Snail expression.Genes & genomics · 2022Article
- ARHGAP25 Inhibits Pancreatic Adenocarcinoma Growth by Suppressing Glycolysis via AKT/mTOR Pathway.International journal of biological sciences · 2021Article
- Article
- Modifying the Tumour Microenvironment: Challenges and Future Perspectives for Anticancer Plasma Treatments.Cancers · 2019Review
- The role of TGF-β and its crosstalk with RAC1/RAC1b signaling in breast and pancreas carcinoma.Cell communication and signaling : CCS · 2017Review
- Targeting reactive oxygen species in development and progression of pancreatic cancer.Expert review of anticancer therapy · 2017Review
- Article
- Increasing the endogenous NO level causes catalase inactivation and reactivation of intercellular apoptosis signaling specifically in tumor cells.Redox biology · 2015Article
- Singlet oxygen treatment of tumor cells triggers extracellular singlet oxygen generation, catalase inactivation and reactivation of intercellular apoptosis-inducing signaling.Redox biology · 2015Article
- Article
- Tumor cell-derived MMP3 orchestrates Rac1b and tissue alterations that promote pancreatic adenocarcinoma.Molecular cancer research : MCR · 2014Article
- Oxidative stress and cytokines in the pathogenesis of pancreatic cancer.Journal of cancer prevention · 2014Review
- Regulation of pancreatic cancer growth by superoxide.Molecular carcinogenesis · 2013Article
- NADPH oxidase biology and the regulation of tyrosine kinase receptor signaling and cancer drug cytotoxicity.International journal of molecular sciences · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
K-ras mutations occur in as high as 95% of patients with pancreatic cancer. K-ras activates Rac1-dependent NADPH oxidase, a key source of superoxide. Superoxide has an important function in pancreatic cancer cell proliferation, and scavenging or decreasing the levels of superoxide inhibits pancreatic cancer cell growth both in vitro and in vivo. DNA microarray analysis and RT-PCR has demonstrated that Rac1 is also upregulated in pancreatic cancer. The aim of this study was to determine whether inhibiting Rac1 would alter pancreatic tumor cell behavior. Human pancreatic cancer cells with mutant K-ras (MIA PaCa-2), wild-type K-ras (BxPC-3) and the immortal H6c7 cell line (pancreatic ductal epithelium) expressing K-ras oncogene (H6c7eR-KrasT) that is tumorigenic, were infected with a dominant/negative Rac1 construct (AdN17Rac1). In cells with mutant K-ras, AdN17Rac1 decreased rac activity, decreased superoxide levels and inhibited in vitro growth. However, in the BxPC-3 cell line, AdN17Rac1 did not change rac activity, superoxide levels or in vitro cell growth. Additionally, AdN17Rac1 decreased superoxide levels and inhibited in vitro growth in the KrasT tumorigenic cell line, but had no effect in the immortalized H6c7 cell line. In human pancreatic tumor xenografts, intratumoral injections of AdN17Rac1 inhibited tumor growth. These results suggest that activation of Rac1-dependent superoxide generation leads to pancreatic cancer cell proliferation. In pancreatic cancer, inhibition of Rac1 may be a potential therapeutic target.
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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.