ArticleJournal of cellular biochemistry2009
Inactivation of uPA and its receptor uPAR by 3,3'-diindolylmethane (DIM) leads to the inhibition of prostate cancer cell growth and migration.
Article in Journal of cellular biochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 51 citations in OpenAlex.
- Angelicin Inhibits NSCLC Tumor Growth via the Inhibition of Cancer-Associated Fibroblasts.Combinatorial chemistry & high throughput screening · 2026Article
- Review
- Article
- Regulation of carcinogenesis and mediation through Wnt/β-catenin signaling by 3,3'-diindolylmethane in an enzalutamide-resistant prostate cancer cell line.Scientific reports · 2021Article
- Recent progress in natural dietary non-phenolic bioactives on cancers metastasis.Journal of food and drug analysis · 2018Review
- A novel peptide blocking cancer cell invasion by structure-based drug design.Biomedical reports · 2017Article
- Cellular and Molecular Mechanisms of 3,3'-Diindolylmethane in Gastrointestinal Cancer.International journal of molecular sciences · 2016Review
- Roles of Dietary Phytoestrogens on the Regulation of Epithelial-Mesenchymal Transition in Diverse Cancer Metastasis.Toxins · 2016Review
- 3'3-Diindolylmethane inhibits migration, invasion and metastasis of hepatocellular carcinoma by suppressing FAK signaling.Oncotarget · 2015Article
- Elongation factor-2 kinase regulates TG2/β1 integrin/Src/uPAR pathway and epithelial-mesenchymal transition mediating pancreatic cancer cells invasion.Journal of cellular and molecular medicine · 2014Article
- Multiple therapeutic and preventive effects of 3,3'-diindolylmethane on cancers including prostate cancer and high grade prostatic intraepithelial neoplasia.Journal of biomedical research · 2014Article
- Recent progress on nutraceutical research in prostate cancer.Cancer metastasis reviews · 2014Review
- Advances in androgen receptor targeted therapy for prostate cancer.Journal of cellular physiology · 2014Review
- Systems and Network Pharmacology Approaches to Cancer Stem Cells Research and Therapy.Journal of stem cell research & therapy · 2012Article
- Natural compounds as anticancer agents: Experimental evidence.World journal of experimental medicine · 2012Review
- Mechanisms and functional consequences of PDEF protein expression loss during prostate cancer progression.The Prostate · 2011Article
- RETRACTED: Mechanisms and therapeutic implications of cell death induction by indole compounds.Cancers · 2011Article
- Spontaneous regression of septum pellucidum/forniceal pilocytic astrocytomas--possible role of Cannabis inhalation.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2011Article
- Novel targets for prostate cancer chemoprevention.Endocrine-related cancer · 2010Review
- PAR-4 as a possible new target for pancreatic cancer therapy.Expert opinion on therapeutic targets · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
3,3'-Diindolylmethane (DIM) has been studied for its putative anti-cancer properties, especially against prostate cancer; however, its exact mechanism of action remains unclear. We recently provided preliminary data suggesting down-regulation of uPA during B-DIM (a clinically active DIM)-induced inhibition of invasion and angiogenesis in prostate cancer cells. Since the expression and activation of uPA plays important role in tumorigenicity, and high endogenous levels of uPA and uPAR are found in advanced metastatic cancers, we investigated their role in B-DIM-mediated inhibition of prostate cancer cell growth and motility. Using PC3 cells, we found that B-DIM treatment as well as the silencing of uPA and uPAR by siRNAs led to the inhibition of cell growth and motility. Conversely, over-expression of uPA/uPAR in LNCaP and C4-2B cells resulted in increased cell growth and motility, which was effectively inhibited by B-DIM. Moreover, we found that uPA as well as uPAR induced the production of VEGF and MMP-9, and that the down-regulation of uPA/uPAR by siRNAs or B-DIM treatment resulted in the inhibition of VEGF and MMP-9 secretion which could be responsible for the observed inhibition of cell migration. Interestingly, silencing of uPA/uPAR led to decreased sensitivity to B-DIM indicating important role of uPA/uPAR in B-DIM-mediated regulation of prostate cancer cell growth and migration. Our data suggest that chemopreventive and/or therapeutic activity of B-DIM is in part due to down-regulation of uPA-uPAR leading to reduced production of VEGF/MMP-9 which ultimately leads to the inhibition of cell growth and migration of aggressive prostate cancer cells.
Indexed as
Identifiers
What 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.