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

Wen Shih Huang, Cheng Nan Chen, Chun-I Sze, Chih Chuan Teng

研究成果: Article

24 引文 (Scopus)

摘要

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. J. Cell. Physiol.

原文English
頁(從 - 到)1017-1024
頁數8
期刊Journal of Cellular Physiology
228
發行號5
DOIs
出版狀態Published - 2013 五月 1

指紋

Nicotinamide Phosphoribosyltransferase
Chemokine CXCL12
Integrins
Colorectal Neoplasms
Cells
Adipokines
Transcription Factor AP-1
Chemical activation
Critical Pathways
Biomarkers
p38 Mitogen-Activated Protein Kinases
Luciferases
Small Interfering RNA
Adipose Tissue
Assays
Transcription Factors
Obesity
Enzyme-Linked Immunosorbent Assay
Tissue

All Science Journal Classification (ASJC) codes

  • Clinical Biochemistry
  • Cell Biology
  • Physiology

引用此文

Huang, Wen Shih ; Chen, Cheng Nan ; Sze, Chun-I ; Teng, Chih Chuan. / Visfatin induces stromal cell-derived factor-1 expression by β1 integrin signaling in colorectal cancer cells. 於: Journal of Cellular Physiology. 2013 ; 卷 228, 編號 5. 頁 1017-1024.
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abstract = "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. J. Cell. Physiol.",
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Visfatin induces stromal cell-derived factor-1 expression by β1 integrin signaling in colorectal cancer cells. / Huang, Wen Shih; Chen, Cheng Nan; Sze, Chun-I; Teng, Chih Chuan.

於: Journal of Cellular Physiology, 卷 228, 編號 5, 01.05.2013, p. 1017-1024.

研究成果: Article

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