Urokinase induces stromal cell‐derived factor‐1 expression in human hepatocellular carcinoma cells

Hsu, Wen Lin; Chen, Cheng‐Nan; Huang, Hai-I; Lai, Yi-Liang; Teng, Chun-Yuh; Kuo, Wu‐Hsien

doi:10.1002/jcp.22777

Cited by 12 publications

(9 citation statements)

References 32 publications

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“…The activation of the SP-1 downstream of the MAPK or PI3K-Akt pathways is involved in numerous pathological processes, such as inflammation, cancer-cell adhesion, tumor invasion, metastasis, and angiogenesis [23], [33]. Hsu et al reported on the u-PA upregulation by stromal cell-derived factor-1 through ERK and JNK phosphorylation with the modulation of the transcription factors SP-1 and AP-1 activity [34]. In this study, we found that resveratrol inhibited the binding activity of SP-1 to the u-PA promoter in Huh7 cells.…”

Section: Discussionmentioning

confidence: 99%

The Antimetastatic Effects of Resveratrol on Hepatocellular Carcinoma through the Downregulation of a Metastasis-Associated Protease by SP-1 Modulation

et al. 2013

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BackgroundThe mortality and morbidity rates from cancer metastasis have not declined in Taiwan, especially because of hepatocellular carcinoma (HCC). Resveratrol has been shown to have benefits such as cardioprotection, providing antioxidative, anti-inflammatory, anti-cancer properties in previous studies. Therefore, HCC cells were subjected to treatment with resveratrol and then analyzed to determine the effects of resveratrol on the migration and invasion.Methodology and Principal FindingsModified Boyden chamber assays revealed that resveratrol treatment significantly inhibited cell migration and invasion capacities of Huh7 cell lines that have low cytotoxicity in vitro, even at a high concentration of 100 µM. The results of casein zymography and western blotting revealed that the activities and protein levels of the urokinase-type plasminogen activator (u-PA) were inhibited by resveratrol. Western blot analysis also showed that resveratrol inhibits phosphorylation of JNK1/2. Tests of the mRNA level, real-time PCR, and promoter assays evaluated the inhibitory effects of resveratrol on u-PA expression in HCC cells. The chromatin immunoprecipitation (ChIP) assay showed that reactive in transcription protein of nuclear factor SP-1 was inhibited by resveratrol.ConclusionsResveratrol inhibits u-PA expression and the metastasis of HCC cells and is a powerful chemopreventive agent. The inhibitory effects were associated with the downregulation of the transcription factors of SP-1 signaling pathways.

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Section: Discussionmentioning

confidence: 99%

The Antimetastatic Effects of Resveratrol on Hepatocellular Carcinoma through the Downregulation of a Metastasis-Associated Protease by SP-1 Modulation

et al. 2013

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“…Moreover, AP‐1 activity can be regulated by altering the expression of specific AP‐1 components as a result of the activation of intracellular signaling cascades (Kundu et al, 2006). Previous study also demonstrated that the activation of the ERK pathway is critical for SDF‐1 expression in hepatocellular carcinoma cells (Hsu et al, 2012). Another study showed that SDF‐1 up‐regulation in cardiac cells was counteracted by a p38 inhibitor (Hohensinner et al, 2009).…”

Section: Discussionmentioning

confidence: 75%

Visfatin induces stromal cell‐derived factor‐1 expression by β1 integrin signaling in colorectal cancer cells

Huang

Chen

Sze

et al. 2013

Journal Cellular Physiology

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Obesity has been shown to be associated with the risk of colorectal cancer (CRC). Adipokines produced by the adipose tissue are linked to some malignancies, including CRC. Visfatin is an adipokine shown to be a biomarker of CRC malignant potential. In addition, the stromal cell-derived factor-1 (SDF-1) has been reported to play a role in CRC progression. Although the relationship between visfatin and CRC has been established, the underlying mechanism has not been clarified. We investigated the molecular mechanism governing the interaction between visfatin stimulation and SDF-1 expression in human CRC cell lines. We found that visfatin stimulation led to an increase in the expression and secretion of SDF-1 in CRC DLD-1 and SW48 cells. Experiments involving specific inhibitors and small interfering RNA demonstrated that the activation of ERK and p38 mitogen-activated protein kinase (MAPK) pathways are critical for visfatin-induced SDF-1 expression. Analysis of transcription factor binding using ELISA and luciferase reporter assays revealed that visfatin increased NF-κB- and AP-1-DNA-binding activities in DLD-1 cells. Inhibition of NF-κB and AP-1 activation blocked the visfatin-induced expression and activity of the SDF-1 promoter. The effect of visfatin on DLD-1 signaling and SDF-1 expression was mediated by β1 integrin. In summary, these findings provide novel insights pertaining to the pathophysiological role of visfatin in CRC.

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“…148 Moreover, the CXCL12/CXCR4 axis was found to cross talk with other relevant intrahepatic pathways, including osteopontin and urokinase. 149,150 More recently, this system has also been linked to the biology of tumor-initiating cells expressing the progenitor marker OV6. CXCL12 provoked an expansion of the OV6-positive population and sustained their stemness properties, 151 while receptor antagonist or CXCR4 small interfering RNAs blocked these effects.…”

Section: Progression and Regression Of Fibrosismentioning

confidence: 99%

Roles for Chemokines in Liver Disease

2014

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Urokinase induces stromal cell‐derived factor‐1 expression in human hepatocellular carcinoma cells

Cited by 12 publications

References 32 publications

The Antimetastatic Effects of Resveratrol on Hepatocellular Carcinoma through the Downregulation of a Metastasis-Associated Protease by SP-1 Modulation

The Antimetastatic Effects of Resveratrol on Hepatocellular Carcinoma through the Downregulation of a Metastasis-Associated Protease by SP-1 Modulation

Visfatin induces stromal cell‐derived factor‐1 expression by β1 integrin signaling in colorectal cancer cells

Roles for Chemokines in Liver Disease

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