PMA-induced up-regulation of MMP-9 is regulated by a PKCα-NF-κB cascade in human lung epithelial cells

Shin, Yoonseok; Yoon, Soo-Han; Choe, Eun Young; Cho, Sung Hoon; Woo, Chang Hoon; Rho, Jee Yeon; Kim, Jae Hong

doi:10.1038/emm.2007.11

Cited by 98 publications

(76 citation statements)

References 45 publications

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“…Activation of PKC by TPA is critical for tumor invasion and MMP-9 induction (7,29). Our previous study showed that activation of PKCa by TPA induced the proliferation and secretion of MMP-2 in fibroblasts and colorectal carcinoma cells (25,30).…”

Section: Discussionmentioning

confidence: 99%

Heme oxygenase-1 inhibits breast cancer invasion via suppressing the expression of matrix metalloproteinase-9

Lin¹,

Shen

Hou

et al. 2008

Molecular Cancer Therapeutics

112

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In the present study, we investigated the antitumor effects of the invasiveness and migration of heme oxygenase 1 (HO-1) in human breast carcinoma cells. 12-O-tetradecanoylphorbol-13-acetate (TPA) -induced matrix metalloproteinase-9 (MMP-9) enzyme activity and gene expression at both protein and mRNA levels were examined in human breast carcinoma cells (MCF-7 and MDA-MB-231), and the addition of the MMP-9 inhibitor, SB3CT, significantly suppressed TPA-induced invasion and migration according to the in vitro Transwell assay. Elevation of HO-1 gene expression by ferric protoporphyrin IX inhibited TPA-induced invasion of MCF-7 cells, which was blocked by adding the heme oxygenase inhibitor, tin protoporphyrin IX, or transfection of cells with HO-1 short hairpin RNA. MCF-7 cells overexpressing HO-1 (MCF-7/HO-1) were established in the present study, and TPA-induced MMP-9 gene expression, tumor invasion, and colony formation were significantly reduced in MCF-7/HO-1 cells, compared with those in Neo-transfected cells. Activation of protein kinase CA/extracellular signalregulated kinases/AP-1 with stimulation of reactive oxygen species production was involved in TPA-induced invasion of MCF-7 cells, which was attenuated by HO-1 protein induced by ferric protoporphyrin IX or transfection of HO-1 expression vectors. Additionally, the addition of carbon monoxide, but not ferric ions, biliverdin, or bilirubin, inhibited TPA-induced invasion through suppressing MMP-9, extracellular signal-regulated kinases, and AP-1 activation stimulated by TPA. The beneficial role of HO-1 in blocking tumor invasion was first identified in this study.

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Section: Discussionmentioning

confidence: 99%

Heme oxygenase-1 inhibits breast cancer invasion via suppressing the expression of matrix metalloproteinase-9

Lin¹,

Shen

Hou

et al. 2008

Molecular Cancer Therapeutics

112

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“…The resultant supernatants were assayed for protein and β-galactosidase activity. Luciferase activity was assayed in 10-μl samples of extract; the luciferase luminescence was counted in luminometer (Turner Design, TD-20/20) and normalized to the co-transfected β-galactosidase activity, as described elsewhere (Woo et al, 2000b;Chung et al, 2005;Shin et al, 2007). Transfection experiments were performed in triplicate with two independently isolated sets of cells, and the results were averaged.…”

Section: Transient Transfection and Nf-κb Luciferase Activity Assaymentioning

confidence: 99%

TNF-α-induced up-regulation of intercellular adhesion molecule-1 is regulated by a Rac-ROS-dependent cascade in human airway epithelial cells

et al. 2008

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Up-regulation of intercellular adhesion molecule-1 (ICAM-1) in the lung airway epithelium is associated with the epithelium-leukocyte interaction, critical for the pathogenesis of various lung airway inflammatory diseases such as asthma. However, little is known about how ICAM-1 is up-regulated in human airway epithelial cells. In this study, we show that tumor TNF-α induces monocyte adhesion to A549 human lung airway epithelium and also up-regulation of ICAM-1 expression. These effects were significantly diminished by pre-treatment with diphenyliodonium (DPI), an inhibitor of NADPH oxidase-like flavoenzyme. In addition, the level of reactive oxygen species (ROS) was increased in response to TNF-α in A549 cells, suggesting a potential role of ROS in the TNF-α-induced signaling to ICAM-1 expression and monocyte adhesion to airway epithelium. Further, we found out that expression of Rac

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“…Activation of pro-inflammatory pathways in lung epithelial cells, including the PKC, AP-1, and NF-kB pathways, by bacterial infection are suggested to contribute significantly to pneumonia [4,10,26]. Although L. pneumophila efficiently infects and stimulates lung epithelial cells [4][5][6][7] and GM-CSF has been shown as important for bacteria elimination via phagocytosis, mechanisms of L. pneumophila-induced release of this cytokine are widely unknown.…”

mentioning

confidence: 99%

“…The expression of GM-CSF is controlled by a tight regulatory network involving the transcription-factors nuclear factor (NF)-kB and the activator protein (AP)-1 [24,25]. These transcription factors are activated by complex signalling pathways, including protein kinase C (PKC) [26,27]. PKCs, a family of serine/threonine kinases, are involved in different biological processes.…”

mentioning

confidence: 99%

PKCα and PKCϵ differentially regulateLegionella pneumophila-induced GM-CSF

Vardarova

Scharf²,

Lang³

et al. 2009

Eur Respir J

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Legionella pneumophila is an important causative agent of severe pneumonia in humans. The human alveolar epithelium is an effective barrier for inhaled microorganisms and actively participates in the initiation of innate host defense. Although secretion of granulocytemacrophage colony-stimulating factor (GM-CSF) is essential for the elimination of invading Legionella spp., mechanisms of Legionella pneumophila-induced release of this cytokine are widely unknown.In this study, we have demonstrated a toll-like receptor (TLR)2-and TLR5-dependent release of GM-CSF in L. pneumophila-infected human alveolar epithelial cells. GM-CSF secretion was not dependent on the bacteria type II or type IV secretion system. Furthermore, an increase in protein kinase C (PKC) activity, particularly PKCa and PKCe, was noted. Blocking of PKCa and PKCe activity or expression, but not of PKCb, PKCd, PKCg, PKCh, and PKCf, significantly reduced the synthesis of GM-CSF in infected cells. While PKCa was critical for the initiation of a nuclear factorkB-mediated GM-CSF expression, PKCe regulated GM-CSF production via activator protein 1.Thus, differential regulation of GM-CSF, production by PKC isoforms, contributes to the host response in Legionnaires' disease.

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PMA-induced up-regulation of MMP-9 is regulated by a PKCα-NF-κB cascade in human lung epithelial cells

Cited by 98 publications

References 45 publications

Heme oxygenase-1 inhibits breast cancer invasion via suppressing the expression of matrix metalloproteinase-9

Heme oxygenase-1 inhibits breast cancer invasion via suppressing the expression of matrix metalloproteinase-9

TNF-α-induced up-regulation of intercellular adhesion molecule-1 is regulated by a Rac-ROS-dependent cascade in human airway epithelial cells

PKCα and PKCϵ differentially regulateLegionella pneumophila-induced GM-CSF

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