Activation of PAR2 or/and TLR4 promotes SW620 cell proliferation and migration via phosphorylation of ERK1/2

Zhou, Beixian; Zhou, Hong; Shucai, Ling; Guo, Dan; Yi, Yan; Zhou, Fang; Wu, Ying

doi:10.3892/or.2010.1077

Cited by 36 publications

(29 citation statements)

References 35 publications

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“…When the cells were pre-incubated with EGCG (100 µg/mL), PAR2-AP-or factor VIIa-induced TF activity and MMP-9 expression were markedly decreased (P<0.01 vs PAR2-AP or factor VIIa alone), as shown in the black column in Figures 4A and 4B. EGCG alone seemed to Effects of EGCG on activation of ERK1/2 and NF-κB in SW620 cells Previously, we found that PAR2-AP and factor VIIa stimulated the activation of ERK1/2 and NF-κB (p65/RelA) in SW620 cells within 30 min of treatment [14,15] . In this study, we further investigated whether EGCG could influence the effects of PAR2-AP and factor VIIa on the levels of p-ERK1/2 and NF-κB (p65/RelA) in the cells.…”

Section: Effects Of Egcg On the Expression Of Tf And Mmp-9 In Sw620 Cmentioning

confidence: 68%

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Epigallocatechin-3-gallate inhibits proliferation and migration of human colon cancer SW620 cells in vitro

Zhou

Wang

et al. 2011

Acta Pharmacol Sin

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Aim: Epigallocatechin-3-gallate (EGCG) is the major polyphenolic constituent in green tea. The aim of this study is to investigate the effects of EGCG on proliferation and migration of the human colon cancer SW620 cells. Methods: Proliferation and migration of SW620 cells were induced by the protease-activated receptor 2-agonist peptide (PAR2-AP, 100 μmol/L) or factor VIIa (10 nmol/L), and analyzed using MTT and Transwell assays, respectively. The cellular cytoskeleton was stained with rhodamine-conjugated phalloidin and examined with a laser scanning confocal fluorescence microscope. The expression of caspase-7, tissue factor (TF) and matrix metalloproteinase (MMP)-9 in the cells was examined using QT-PCR, ELISA and Western blot assays. The activation of extracellular signal-regulated kinase 1 and 2 (ERK1/2) and nuclear factor-kappa B (NF-κB) signaling pathways was analyzed with Western blot. Results: Both PAR2-AP and factor VIIa promoted SW620 cell proliferation and migration, and caused cytoskeleton reorganization (increased filopodia and pseudopodia). Pretreatment with EGCG (25, 50, 75, and 100 μg/mL) dose-dependently blocked the cell proliferation and migration induced by PAR2-AP or factor VIIa. EGCG (100 μg/mL) prevented the cytoskeleton changes induced by PAR2-AP or factor VIIa. EGCG (100 μg/mL) counteracted the down-regulation of caspase-7 expression and up-regulation of TF and MMP-9 expression in the cells treated with PAR2-AP or factor VIIa. Furthermore, it blocked the activation of ERK1/2 and NF-κB (p65/RelA) induced by PAR2-AP or factor VIIa. Conclusion: EGCG blocks the proliferation and migration of SW620 cells induced by PAR2-AP and factor VIIa via inhibition of the ERK1/2 and NF-κB pathways. The compound may serve as a preventive and therapeutic agent for colon cancers.

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Section: Effects Of Egcg On the Expression Of Tf And Mmp-9 In Sw620 Cmentioning

confidence: 68%

“…Factor VIIa can activate PAR2 and promote SW620 cell proliferation and migration in a TF-dependent manner. Some intracellular signaling molecules, such as ERK1/2 and NF-κB, are activated in these processes [9,14,15] . The anti-tumor properties of EGCG have received much attention in recent years.…”

Section: Discussionmentioning

confidence: 99%

Epigallocatechin-3-gallate inhibits proliferation and migration of human colon cancer SW620 cells in vitro

Zhou

Wang

et al. 2011

Acta Pharmacol Sin

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“…Tremendous undesired effects, and in particular severe metabolic toxicity similar to diabetes mellitus complications, were expected from these molecules that tend to inhibit all ILP activity. Instead, evidence from early clinical experience indicates that these agents are safe and, therefore, promising, given their broader range of receptor inhibition , Zhou et al 2011. The mechanisms explaining the absence of the expected side effects still are to be unraveled, even though some plausible explanations have been suggested.…”

Section: Insulin Resistance Infection and Cancermentioning

confidence: 99%

Insulin resistance and cancer: the role of insulin and IGFs

Djiogue¹,

Kamdje²,

Vecchio³

et al. 2012

Endocrine-Related Cancer

232

188

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Insulin, IGF1, and IGF2 are the most studied insulin-like peptides (ILPs). These are evolutionary conserved factors well known as key regulators of energy metabolism and growth, with crucial roles in insulin resistance-related metabolic disorders such as obesity, diseases like type 2 diabetes mellitus, as well as associated immune deregulations. A growing body of evidence suggests that insulin and IGF1 receptors mediate their effects on regulating cell proliferation, differentiation, apoptosis, glucose transport, and energy metabolism by signaling downstream through insulin receptor substrate molecules and thus play a pivotal role in cell fate determination. Despite the emerging evidence from epidemiological studies on the possible relationship between insulin resistance and cancer, our understanding on the cellular and molecular mechanisms that might account for this relationship remains incompletely understood. The involvement of IGFs in carcinogenesis is attributed to their role in linking high energy intake, increased cell proliferation, and suppression of apoptosis to cancer risks, which has been proposed as the key mechanism bridging insulin resistance and cancer. The present review summarizes and discusses evidence highlighting recent advances in our understanding on the role of ILPs as the link between insulin resistance and cancer and between immune deregulation and cancer in obesity, as well as those areas where there remains a paucity of data. It is anticipated that issues discussed in this paper will also recover new therapeutic targets that can assist in diagnostic screening and novel approaches to controlling tumor development.

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“…This promoted VEGF expression and resistance to apoptosis. Similarly, in SW620 cells (colon cancer cell line), TLR4 promoted cell proliferation and migration through phosphorylation of ERK 1/2 (Zhou et al 2011). Downregulation of TLR4 with siRNA inhibited prostate cancer cell invasion and survival (Hua et al 2009).…”

Section: Discussionmentioning

confidence: 99%

TLR4 mutation and HSP60-induced cell death in adult mouse cardiac myocytes

Heiserman

Chen

Kim

et al. 2015

Cell Stress and Chaperones

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Extracellular (ex) HSP60 is increasingly recognized as an agent of cell injury. Previously, we reported that low endotoxin exHSP60 causes cardiac myocyte apoptosis. Our findings supported a role for Toll-like receptor (TLR) 4 in HSP60 mediated apoptosis. To further investigate the involvement of TLR4 in cardiac injury, we studied adult cardiac myocytes from C3H/HeJ (HeJ) mice, which have a mutant, nonfunctional TLR4, and compared the results with parallel studies using wild-type (WT) mice. Nuclear factor κB (NFκB) activation is an early step downstream of TLR4. NFκB was activated 1 h after treatment with HSP60 in WT, but not HeJ mouse myocytes. ExHSP60 caused apoptosis in cardiac myocytes from WT mice, but not in myocytes from the HeJ mutants. To further elucidate the importance of exHSP60 in cardiac myocyte injury, both WT and HeJ mutant isolated mouse adult cardiac myocytes were exposed to hypoxia/reoxygenation. Anti-HSP60 antibody treatment reduced apoptosis in the WT group, but had no effect on the HeJ mutant myocytes. Unexpectedly, necrosis was also decreased in the HeJ mutants. Necrosis after hypoxia/reoxygenation in WT cardiac myocytes was mediated in part by TLR2 and TLR4 through rapid activation of PKCα, followed by increased expression of Nox2, and this was ameliorated by blocking antibodies to TLR2/4. These studies provide further evidence that TLR4 mediates exHSP60-associated apoptosis and that exHSP60 has an important role in cardiac myocyte injury, both apoptotic and necrotic.

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Activation of PAR2 or/and TLR4 promotes SW620 cell proliferation and migration via phosphorylation of ERK1/2

Cited by 36 publications

References 35 publications

Epigallocatechin-3-gallate inhibits proliferation and migration of human colon cancer SW620 cells in vitro

Epigallocatechin-3-gallate inhibits proliferation and migration of human colon cancer SW620 cells in vitro

Insulin resistance and cancer: the role of insulin and IGFs

TLR4 mutation and HSP60-induced cell death in adult mouse cardiac myocytes

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