Carnosol inhibits the invasion of B16/F10 mouse melanoma cells by suppressing metalloproteinase-9 through down-regulating nuclear factor-kappaB and c-Jun

Huang, Shiu Chen; Ho, Chi‐Tang; Lin‐Shiau, Shoei‐Yn; Lin, Ju‐Li

doi:10.1016/j.bcp.2004.09.019

Cited by 187 publications

(132 citation statements)

References 36 publications

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“…This pathway also exists in the other cell models. Huang et al (2005) showed the inhibitory effect of carnosol on melanoma cell migration and invasion occurred mainly as a result of reduced MMP-9 expression, which was mediated through suppressing the ERK1/2, Akt, p38 and JNK pathways and inhibiting NF-kB-and AP-1-binding activities. Moreover, Agarwal et al (2005) found that PI3K/Akt/IkB pathway positively regulated NF-kB and b-catenin in colorectal cancer cells, and using array analysis, that most of the PI3K/Akt/IkB genes are involved in tumor angiogenesis and metastasis.…”

Section: Discussionmentioning

confidence: 99%

Radiation-enhanced hepatocellular carcinoma cell invasion with MMP-9 expression through PI3K/Akt/NF-κB signal transduction pathway

et al. 2006

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This study is to investigate the molecular mechanism of radiation-enhanced cell invasiveness of hepatocellular carcinoma (HCC) correlating with clinical patients undergoing radiotherapy and subsequently developing metastasis. Three HCC cell lines (HepG2, Hep3B and Huh7) and normal hepatocyte cell line (CL-48) were irradiated with different doses. The effect of radiation on cell invasiveness was determined using the Boyden chamber assay. Radiation-enhanced invasion capability was evident in HCC cells but not in normal hepatocytes. Invasion was observed in gelatin-coated but not fibronectin-coated or type I collagen-coated membranes. Radiation upregulated matrix metalloproteinase-9 (MMP-9) mRNA level, MMP-9 protein level and MMP-9 activity. MMP-9 antisense oligonucleotides inhibited radiation-induced MMP-9 expression and thereby significantly inhibited radiationinduced HCC invasion. Furthermore, phosphatidylinositol 3-kinase (PI3K)/Akt chemical inhibitors LY294002 and wortmannin suppressed radiation-induced MMP-9 mRNA expression. Transient transfection with dominantnegative Akt plasmid also showed that the PI3K/Aktsignaling pathway was involved in this radiation-induced MMP-9 expression. Moreover, nuclear factor-jB (NFjB) decoy oligodeoxynucleotide suppressed radiation enhanced MMP-9 promoter activity completely. PI3K/ Akt chemical inhibitors inhibited radiation-induced NFjB-driven luciferase promoter activity. Taken together, our results indicated that sublethal dose of radiation could enhance HCC cell invasiveness by MMP-9 expression through the PI3K/Akt/NF-jB signal transduction pathway.

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Section: Discussionmentioning

confidence: 99%

Radiation-enhanced hepatocellular carcinoma cell invasion with MMP-9 expression through PI3K/Akt/NF-κB signal transduction pathway

et al. 2006

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“…19 Resveratrol, in turn, blocks TNFa-induced NF-kB activation in U-937 myeloid, Jurkat lymphoid, and epithelial HeLa and H4 cells, 20 while carnosol blocks NF-kB translocation and DNA binding in LPS-activated mouse macrophages 21 and in B16/F10 mouse melanoma cells. 22 Phenolic acids and their analogs (Table I) can also act through this chemopreventive mechanism. 12,13…”

Section: A Suppression Of Nf-k Kb Transcription Factor Activationmentioning

confidence: 99%

New insights on the anticancer properties of dietary polyphenols

et al. 2006

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Cancer, one of the major causes of death across the world, has shown to be a largely preventable disease, highly susceptible to modulation by dietary factors. Phenolic compounds, abundant in vegetables and fruits ubiquitous in diet, were described to play an important role as chemopreventive agents. Since conventional therapeutic and surgical approaches have not been able to control the incidence of most cancer types, the development of chemopreventive strategies is an urgent priority in public health. The current diet phenolic intake is often insufficient to protect from mutagens (either exogenous or endogenous), which leads to the need for dietary supplementation as an alternative approach. Research efforts are placing increasing emphasis on identifying the biological mechanisms and in particular the signal transduction pathways related to the chemopreventive activities of these compounds. These effects are believed to occur by the regulation of signaling pathways such as nuclear factor-kB (NF-kB), activator protein-1 (AP-1) or mitogen-activated protein kinases (MAPK). Dietary polyphenols can exert their effects on these pathways separately or sequentially and in addition the occurrence of crosstalk between these pathways cannot be overlooked. By modulating cell signaling pathways, polyphenols activate cell death signals and induce apoptosis in precancerous or malignant cells resulting in the inhibition of cancer development or progression. However, regulation of cell signaling pathways by dietary polyphenols can also lead to cell proliferation/survival or inflammatory responses due to increased expression of several genes. The present review summarizes the most recent advances providing new insights into the molecular mechanisms underlying the promising anticarcinogenic activity of dietary polyphenols. ß

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“…Enzymatic degradation of ECM is a crucial step in cancer invasion and metastasis (3,4). MMPs play a key role in carcinogenesis.…”

Section: Discussionmentioning

confidence: 99%

“…As cancer cells become metastatic and endothelial cells angiogenic, they develop altered affinity and avidity for their extracellular matrix (ECM; ref. 3). The degradation of basement membranes and stromal ECM are crucial in tumor invasion and metastasis.…”

Section: Introductionmentioning

confidence: 99%

Rho Guanine Nucleotide Exchange Factor 5 Increases Lung Cancer Cell Tumorigenesis via MMP-2 and Cyclin D1 Upregulation

Yang

et al. 2015

Molecular Cancer Therapeutics

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We sought to elucidate the role of Rho guanine nucleotide exchange factor 5 (ARHGEF5) in tumorigenesis of lung adenocarcinoma cells. ARHGEF5 protein levels were assessed in 91 human lung adenocarcinoma specimens, and A549 and NCI-H1650 cells, by IHC and Western blotting. In addition, ARHGEF5 mRNA expression was evaluated by quantitative reverse transcriptase-PCR. Furthermore, ARHGEF5 long and short isoform coexpression was detected by immunofluorescence. Finally, flow cytometry; CCK8 and wound-healing assays; cell invasion, migration and adhesion; and xenografts were used to evaluate the biologic significance of ARHGEF5. ARHGEF5 was significantly increased in lung adenocarcinoma tissues and cell lines. Interestingly, ARHGEF5 levels were significantly associated with tumor grade and pathologic stage, but not age, gender, T stage, or lymph node metastasis status. ARHGEF5 knockdown by RNAi resulted in dramatically reduced proliferation, adhesion, invasion, and migratory capability of A549 and NCI-H1650 cells. Likewise, protein levels of p-Src, p-Akt, and NF-kB were significantly decreased after ARHGEF5 knockdown. In parallel, increased S-phase population and MMP-2/cyclin D1 expression were observed in the cancer cells, which were not apoptotic. In addition, ARHGEF5 knockdown A549 and NCI-H1650 cells injected s.c. and i.v. into nude mice exhibited decreased xenograft volume and overtly reduced metastasis. Conversely, ARH-GEF5 overexpression in A549 and NCI-H1650 cells increased their tumorigenicity in vitro. ARHGEF5 acts as a proto-oncogene in human lung adenocarcinoma cell tumorigenesis.

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Carnosol inhibits the invasion of B16/F10 mouse melanoma cells by suppressing metalloproteinase-9 through down-regulating nuclear factor-kappaB and c-Jun

Cited by 187 publications

References 36 publications

Radiation-enhanced hepatocellular carcinoma cell invasion with MMP-9 expression through PI3K/Akt/NF-κB signal transduction pathway

Radiation-enhanced hepatocellular carcinoma cell invasion with MMP-9 expression through PI3K/Akt/NF-κB signal transduction pathway

New insights on the anticancer properties of dietary polyphenols

Rho Guanine Nucleotide Exchange Factor 5 Increases Lung Cancer Cell Tumorigenesis via MMP-2 and Cyclin D1 Upregulation

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