NDLI: Camptothecin suppresses expression of matrix metalloproteinase-9 and vascular endothelial growth factor in DU145 cells through PI3K/Akt-mediated inhibition of NF-κB activity and Nrf2-dependent induction of HO-1 expression.

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Camptothecin suppresses expression of matrix metalloproteinase-9 and vascular endothelial growth factor in DU145 cells through PI3K/Akt-mediated inhibition of NF-κB activity and Nrf2-dependent induction of HO-1 expression.

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Camptothecin suppresses expression of matrix metalloproteinase-9 and vascular endothelial growth factor in DU145 cells through PI3K/Akt-mediated inhibition of NF-κB activity and Nrf2-dependent induction of HO-1 expression.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Jayasooriya, Rajapaksha Gedara Prasad Tharanga Park, Sang Rul Choi, Yung Hyun Hyun, Jin-Won Chang, Weon-Young Kim, Gi-Young
Description	Author Affiliation: Jayasooriya RG ( Department of Marine Life Sciences, Jeju National University, Ara-1 dong, Jeju 690-756, Republic of Korea.); Park SR ( Department of Marine Life Sciences, Jeju National University, Ara-1 dong, Jeju 690-756, Republic of Korea.); Choi YH ( Department of Biochemistry, College of Oriental Medicine, Dong-Eui University, Busan 614-050, Republic of Korea.); Hyun JW ( School of Medicine, Jeju National University, Jeju-si 690-756, Republic of Korea.); Chang WY ( School of Medicine, Jeju National University, Jeju-si 690-756, Republic of Korea.); Kim GY ( Department of Marine Life Sciences, Jeju National University, Ara-1 dong, Jeju 690-756, Republic of Korea. Electronic address: immunkim@jejunu.ac.kr.)
Abstract	Though camptothecin (CPT) possesses potent anti-inflammatory, immunomodulatory, anticancerous, and antiproliferative effects, little is known about the mechanism by which CPT regulates the expression of matrix metalloproteinase-9 (MMP-9) and vascular endothelial growth factor (VEGF). Therefore, the current study aimed to investigate the effects of CPT on the expression of MMP-9 and VEGF, which are important factors for the invasion of tumors. In vitro application of CPT resulted in a slight inhibition of cell proliferation and a significant reduction in the matrigel invasion of DU145 cells. Treatment with CPT also downregulated phorbol-12-myristate-13-acetate (PMA)- and tumor necrosis factor- (TNF- )-induced MMP-9 and VEGF expression by inhibiting nuclear factor-κB (NF-κB) activity. Downregulation of phosphoinositide 3-kinase (PI3K)/Akt phosphorylation in response to CPT was revealed as an upstream pathway regulating the expression of MMP-9 and VEGF accompanying the inhibition of NF-κB activity. We further confirmed that CPT inhibits PMA-induced MMP-9 and VEGF expression by upregulating nuclear factor-erythroid related factor-2 (Nrf2)-mediated heme oxygenase-1 (HO-1) induction. Taken together, these data indicate that CPT inhibits the invasion of cancer cells accompanied by suppression of MMP-9 and VEGF production by suppressing the PI3K/Akt-mediated NF-κB pathway and enhancing the Nrf2-dependent HO-1 pathway, suggesting that CPT may be a good candidate to inhibit MMP-9 and VEGF expression.
File Format	HTM / HTML
ISSN	13826689
Issue Number	3
Volume Number	39
e-ISSN	18727077
Journal	Environmental Toxicology and Pharmacology
Language	English
Publisher	Elsevier
Publisher Date	2015-05-01
Publisher Place	Netherlands
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Environmental Health Discipline Pharmacology Antineoplastic Agents, Phytogenic Pharmacology Camptothecin Matrix Metalloproteinase 9 Metabolism Prostatic Neoplasms Vascular Endothelial Growth Factor A Cell Line, Tumor Cell Movement Drug Effects Cell Proliferation Gene Expression Regulation, Neoplastic Heme Oxygenase-1 Humans Male Genetics Nf-kappa B Phosphatidylinositol 3-kinases Proto-oncogene Proteins C-akt Signal Transduction Tetradecanoylphorbol Acetate Analogs & Derivatives Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Health, Toxicology and Mutagenesis Medicine Toxicology Pharmacology

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