ArticleMolecular carcinogenesis2014
Induction of reactive oxygen species generation inhibits epithelial-mesenchymal transition and promotes growth arrest in prostate cancer cells.
Article in Molecular carcinogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 79 citations in OpenAlex.
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- Kallistatin Deficiency Induces the Oxidative Stress-Related Epithelial-Mesenchymal Transition of Retinal Pigment Epithelial Cells: A Novel Protagonist in Age-Related Macular Degeneration.Investigative ophthalmology & visual science · 2023Article
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- A small molecule inhibitor of Notch1 modulates stemness and suppresses breast cancer cell growth.Frontiers in pharmacology · 2023Article
- Sinomenine Confers Protection Against Myocardial Ischemia Reperfusion Injury by Preventing Oxidative Stress, Cellular Apoptosis, and Inflammation.Frontiers in pharmacology · 2022Article
- Identification of novel cell glycolysis related gene signature predicting survival in patients with breast cancer.Scientific reports · 2021Article
- Induction of mitochondria mediated apoptosis in human ovarian cancer cells by folic acid coated tin oxide nanoparticles.PloS one · 2021Article
- Chronic exposure to cadmium induces a malignant transformation of benign prostate epithelial cells.Oncogenesis · 2020Article
- Pharmacological Activities of Psoralidin: A Comprehensive Review of the Molecular Mechanisms of Action.Frontiers in pharmacology · 2020Review
- Smart Sorting of Tumor Phenotype with Versatile Fluorescent Ag Nanoclusters by Sensing Specific Reactive Oxygen Species.Theranostics · 2020Article
- Identification of a novel glycolysis-related gene signature for predicting metastasis and survival in patients with lung adenocarcinoma.Journal of translational medicine · 2019Article
- Molecular Pathway of Psoralidin-Induced Apoptosis in HepG2 Cell Line.Chinese journal of integrative medicine · 2019Article
- The chemopreventive effect of withaferin A on spontaneous and inflammation-associated colon carcinogenesis models.Carcinogenesis · 2018Article
- Procyanidin B2 3,3″-di-O-gallate induces oxidative stress-mediated cell death in prostate cancer cells via inhibiting MAP kinase phosphatase activity and activating ERK1/2 and AMPK.Molecular carcinogenesis · 2018Article
- Induction of Plac8 promotes pro-survival function of autophagy in cadmium-induced prostate carcinogenesis.Cancer letters · 2017Article
- EMT and inflammation: inseparable actors of cancer progression.Molecular oncology · 2017Review
- Inhibition of autophagy prevents cadmium-induced prostate carcinogenesis.British journal of cancer · 2017Article
- Targeting aberrant expression of Notch-1 in ALDHMolecular carcinogenesis · 2017Article
- JS-K promotes apoptosis by inducing ROS production in human prostate cancer cells.Oncology letters · 2017Article
- The Effect of CoCellular and molecular bioengineering · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Oxidative stress is one causative factor of the pathogenesis and aggressiveness of most of the cancer types, including prostate cancer (CaP). A moderate increase in reactive oxygen species (ROS) induces cell proliferation whereas excessive amounts of ROS promote apoptosis. In this study, we explored the pro-oxidant property of 3,9-dihydroxy-2-prenylcoumestan (psoralidin [pso]), a dietary agent, on CaP (PC-3 and C4-2B) cells. Pso greatly induced ROS generation (more than 20-fold) that resulted in the growth inhibition of CaP cells. Overexpression of anti-oxidant enzymes superoxide dismutase 1 (SOD1), SOD2, and catalase, or pretreatment with the pharmacological inhibitor N-acetylcysteine (NAC) significantly attenuated both pso-mediated ROS generation and pso-mediated growth inhibition in CaP cells. Furthermore, pso administration significantly inhibited the migratory and invasive property of CaP cells by decreasing the transcription of β-catenin, and slug, which promote epithelial-mesenchymal transition (EMT), and by concurrently inducing E-cadherin expression in CaP cells. Pso-induced ROS generation in CaP cells resulted in loss of mitochondrial membrane potential, cytochrome-c release, and activation of caspase-3 and -9 and poly (ADP-ribose) polymerase (PARP), which led to apoptosis. On the other hand, overexpression of anti-oxidants rescued pso-mediated effects on CaP cells. These findings suggest that increasing the threshold of intracellular ROS could prevent or treat CaP growth and metastasis.
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