Inhibition of EGF/EGFR activation with naphtho[1,2-b]furan-4,5-dione blocks migration and invasion of MDA-MB-231 cells

Hsieh, Chi-Ying; Tsai, Pei‐Chien; Tseng, Chih‐Hua; Chen, Yeh‐Long; Chang, Long‐Sen; Lin, Shinne‐Ren

doi:10.1016/j.tiv.2012.10.001

Cited by 34 publications

(25 citation statements)

References 38 publications

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“…Activation of epidermal growth factor receptor (EGFR)-induced signaling pathway has been correlated with cancer metastasis in various tumors, including breast carcinoma (24). According to the previous reports, exposure of different mammary epithelial cells to epidermal growth factor (EGF) resulted in morphological alterations characteristic of epithelial-tomesenchymal transition (EMT) (25).…”

Section: Smar1 Also Inhibits Egf-mediated Slug Up-regulation To Restomentioning

confidence: 99%

Inhibition of Epithelial to Mesenchymal Transition by E-cadherin Up-regulation via Repression of Slug Transcription and Inhibition of E-cadherin Degradation

Adhikary

Chakraborty

Mazumdar

et al. 2014

Journal of Biological Chemistry

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Background: Epithelial-mesenchymal transition (EMT) is an important program in tumor metastasis. Results: SMAR1 inhibits EMT by up-regulating E-cadherin in a dual manner via repression of Slug transcription and inhibition of E-cadherin degradation. Conclusion: SMAR1 functions as a critical protein in regulating EMT. Significance: This study provides a potential mechanism for the contribution of SMAR1 in inhibiting breast cancer metastasis.

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Section: Smar1 Also Inhibits Egf-mediated Slug Up-regulation To Restomentioning

confidence: 99%

Inhibition of Epithelial to Mesenchymal Transition by E-cadherin Up-regulation via Repression of Slug Transcription and Inhibition of E-cadherin Degradation

Adhikary

Chakraborty

Mazumdar

et al. 2014

Journal of Biological Chemistry

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“…Aberrations in EGFR lead to the abating of downstream signaling molecules such as focal adhesion kinase (FAK), the phosphatidylinositol-3 kinase (PI3K), Ras-mitogen-activated protein kinase (Ras-MAPK) generating an anti-metastatic/invasive effect (13)(14)(15)(16)(17)(18). In addition, GnT-V has been found to contribute to heparin-binding EGF-like growth factor (HB-EGF)-mediated epidermal hyperproliferation by inhibiting endocytosis of EGFRs bearing β1-6 GlcNAc on their N-glycans (19).…”

Section: Introductionmentioning

confidence: 99%

Downregulation of the GnT-V gene inhibits metastasis and invasion of BGC823 gastric cancer cells

et al. 2013

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Abstract. Metastatic and invasive potential is a barrier to the successful treatment of gastric cancer. N-acetylglucosaminyltransferase V (GnT-V), a key enzyme catalyzing the formation of 1,6 N-acetylglucosamine (GlcNAc), has been demonstrated to display a distinct function in different types of tumors. The aim of this study was to investigate the role of GnT-V in the invasive potential of BGC823 human gastric cancer cells in vitro and the possible underlying mechanism. GnT-V was downregulated in BGC823 cells by oligo-siRNA transfection. Cell proliferation and invasiveness were assessed by CCK-8 assay, TUNEL assay, scratch-wound assay as well as Transwell assay. The products of GnT-V, β1-6 branching of asparagine-linked oligosaccharides, were determined by L-PHA lectin blot analysis. The expression of EGFRs, E-cadherin/vimentin and MMP-2/MMP-9 was analyzed both at the mRNA and protein levels. The results showed that downregulation of GnT-V decreased proliferation and the metastatic/invasive potential of BGC823 cells. The expression of EGFRs, E-cadherin/vimentin and MMP-9, molecules related to cancer metastasis and invasion in various tumors, were influenced correspondingly. These findings suggest that downregulation of GnT-V inhibited cell metastasis and invasion of BGC823 cells via EGFR signaling-initiated EMT phenotype and MMP-9 expression. These results provide a novel mechanism to explain the role of GnT-V in cell metastasis and invasion.

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“…18 In addition, we showed that NFD blocks the migration and invasion of MDA-MB-231 cells by suppressing EGF and/or EGFR activation 19 and Src-mediated signalling pathways. 20 The HGF/c-Met signalling pathway is deregulated in most cancers and is associated with poor prognosis in breast cancer.…”

Section: Discussionmentioning

confidence: 86%

Inhibitory action of naphtho[1,2‐b]furan‐4,5‐dione on hepatocyte growth factor‐induced migration and invasion of MDA‐MB‐231 cells: Mechanisms of action

Tsai

Chu

Tseng

et al. 2014

Clin Exp Pharma Physio

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SUMMARYNaphtho [1,2-b]furan-4,5-dione (NFD), a bioactive component of Avicennia marina, has been shown to exhibit anticancer activity. The aim of the present study was to explore the effect of NFD on hepatocyte growth factor (HGF)-induced cell migration and invasion of MDA-MB-231 human breast cancer cells, as well as the underlying mechanism of action. Cell viability was determined using the 3-(4,5-dimethyl-2 thiazoyl)-2,5-diphenyl-2H-tetrazolium bromide assay, western blot analysis was used to measure protein expression and cell migration and invasion were evaluated by the cell wound healing assay, Boyden chamber assay and gelatin zymography. When cells were treated with non-toxic concentrations of NFD (1-3 lmol/L, 24 h), NFD concentration-dependently inhibited HGF-promoted cell migration and invasion. Simultaneously, NFD efficiently suppressed c-Met phosphorylation and downstream activation of phosphatidylinositol 3-kinase (PI3K) and Akt. In addition, NFD inhibited the phosphorylation of IjB kinases and IjBa and nuclear translocation of nuclear factor (NF)-jB, as well as matrix metalloproteinase (MMP)-9 activity. Furthermore, the c-Met inhibitor PHA665752 (10 lmol/L) inhibited HGF-induced MMP-9 expression, cell migration and invasion, as well as the activation of PI3K/Akt, suggesting that PI3K/Akt activation occur downstream of c-Met activation. In conclusion, the results of the present study suggest that NFD inhibits HGF-induced invasion and migration of MDA-MB-231 cells via HGF-and/ or c-Met-mediated PI3K/Akt and NF-jB signalling pathways, leading to downregulation of MMP-9 expression and cell migration.

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Inhibition of EGF/EGFR activation with naphtho[1,2-b]furan-4,5-dione blocks migration and invasion of MDA-MB-231 cells

Cited by 34 publications

References 38 publications

Inhibition of Epithelial to Mesenchymal Transition by E-cadherin Up-regulation via Repression of Slug Transcription and Inhibition of E-cadherin Degradation

Inhibition of Epithelial to Mesenchymal Transition by E-cadherin Up-regulation via Repression of Slug Transcription and Inhibition of E-cadherin Degradation

Downregulation of the GnT-V gene inhibits metastasis and invasion of BGC823 gastric cancer cells

Inhibitory action of naphtho[1,2‐b]furan‐4,5‐dione on hepatocyte growth factor‐induced migration and invasion of MDA‐MB‐231 cells: Mechanisms of action

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