Crude extract of Euphorbia formosana inhibits the migration and invasion of DU145 human prostate cancer cells: The role of matrix metalloproteinase-2/9 inhibition via the MAPK signaling pathway

Yang, Jinghong; Lin, Jing‐Yuan; Weng, Shu Wen; Chen, Jaw Chyun; Yang, Jai Sing; Amagaya, Sakae; Funayana, Shinji; Wood, W. Gibson; Kuo, Chao Lin; Chung, Jing Gung

doi:10.3892/mmr.2013.1380

Cited by 13 publications

(12 citation statements)

References 33 publications

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“…In our study, we found that triticumoside significantly suppressed MMP2/9 mRNA expression in a dose-dependent manner. In line with our results, one study showed that crude extract of Euphorbia formosana inhibits MMP2/9 expression in DU145 human prostate cancer cells to inhibit their migration, suggesting that the extract acts as an antimetastatic agent [20].…”

Section: Discussionsupporting

confidence: 76%

Triticumoside induces apoptosis via caspase-dependent mitochondrial pathway and inhibits migration through downregulation of MMP2/9 in human lung cancer cells

Poudel¹,

Ki²,

Luyen³

et al. 2016

ABBS

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Non-small cell lung cancer (NSCLC) is the major cancer-related death worldwide with only 14% fiveyear survival rate. Triticumoside, a phenolic compound present in Triticum aestivum sprout extract, has been recognized to have antiobesity and anti-inflammatory effects. However, the effect of triticumoside on cancer cell proliferation and migration has not been studied. In order to elucidate whether triticumoside exhibits an anticancer effect, cells were incubated with different doses of triticumoside, and apoptosis was assessed by observing cell viability, cellular morphological changes, and annexin-V-fluorescein isothiocyanate/propidium iodide staining. Cell cycle analysis, western blotting, wound healing assay, and quantitative-polymerase chain reaction were also performed. Triticumoside exhibited marked cytotoxicity in the cells in dose-and time-dependent manner. Triticumoside caused morphological changes, including cellular rounding, nuclear condensation, and shrinkage. Likewise, triticumoside enhanced the sub-G1 proportion of cells. Additionally, triticumoside regulated expression of apoptosis-associated proteins, such as B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X, and procaspase-3/9. Triticumoside also inhibited migration of the cells through downregulation of matrix metalloproteinase-2/9 (MMP2/9). Collectively, these results suggest that triticumoside induces apoptosis through caspase-dependent mitochondrial pathway and suppresses migration via inhibition of MMP2/9 in NSCLC A549 cells.

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Section: Discussionsupporting

confidence: 76%

Triticumoside induces apoptosis via caspase-dependent mitochondrial pathway and inhibits migration through downregulation of MMP2/9 in human lung cancer cells

Poudel¹,

Ki²,

Luyen³

et al. 2016

ABBS

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“…Recent studies showed that SFN inhibited MMP-2 expression in some tumor cell lines [11], [12]. Moreover, our previous studies and others have confirmed that MMP-2 was the downstream effector of ERK1/2 [27], [28], [33], [34]. Therefore, we proposed that SFN might down-regulate MMP-2 via activating ERK1/2 signaling pathway.…”

Section: Introductionmentioning

confidence: 57%

Sulforaphane Inhibits Invasion via Activating ERK1/2 Signaling in Human Glioblastoma U87MG and U373MG Cells

Zhou

Peng

et al. 2014

PLoS ONE

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BackgroundGlioblastoma has highly invasive potential, which might result in poor prognosis and therapeutic failure. Hence, the key we study is to find effective therapies to repress migration and invasion. Sulforaphane (SFN) was demonstrated to inhibit cell growth in a variety of tumors. Here, we will further investigate whether SFN inhibits migration and invasion and find the possible mechanisms in human glioblastoma U87MG and U373MG cells.MethodsFirst, the optimal time and dose of SFN for migration and invasion study were determined via cell viability and cell morphological assay. Further, scratch assay and transwell invasion assay were employed to investigate the effect of SFN on migration and invasion. Meanwhile, Western blots were used to detect the molecular linkage among invasion related proteins phosphorylated ERK1/2, matrix metalloproteinase-2 (MMP-2) and CD44v6. Furthermore, Gelatin zymography was performed to detect the inhibition of MMP-2 activation. In addition, ERK1/2 blocker PD98059 (25 µM) was integrated to find the link between activated ERK1/2 and invasion, MMP-2 and CD44v6.ResultsThe results showed that SFN (20 µM) remarkably reduced the formation of cell pseudopodia, indicating that SFN might inhibit cell motility. As expected, scratch assay and transwell invasion assay showed that SFN inhibited glioblastoma cell migration and invasion. Western blot and Gelatin zymography showed that SFN phosphorylated ERK1/2 in a sustained way, which contributed to the downregulated MMP-2 expression and activity, and the upregulated CD44v6 expression. These molecular interactions resulted in the inhibition of cell invasion.ConclusionsSFN inhibited migration and invasion processes. Furthermore, SFN inhibited invasion via activating ERK1/2 in a sustained way. The accumulated ERK1/2 activation downregulated MMP-2 expression and decreased its activity and upregulated CD44v6. SFN might be a potential therapeutic agent by activating ERK1/2 signaling against human glioblastoma.

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“…MMPs are crucial factors in the invasion and metastasis of prostate cancer cells (13). This study revealed that the overexpression of DUSP6 inhibited MMP-3 expression in DU-145 cells, whereas DUSP6-knockdown enhanced MMP-3 expression in LNCap cells (Fig.…”

Section: Dusp6 Reduces the Expression Of Mmp-3 And Il-8 In Prostate Cmentioning

confidence: 68%

Dual specificity phosphatase 6 suppresses the growth and metastasis of prostate cancer cells

Zhai

Han

Zhang

et al. 2014

Molecular Medicine Reports

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Dual specificity phosphatase 6 (DUSP6) is expressed at low levels in numerous types of human cancer. The loss of DUSP6 plays a pivotal role in tumor progression; however, the role of DUSP6 in prostate cancer remains unclear. In this study, in vitro invasion assays and in vivo metastasis experiments were used to investigate the effects of DUSP6 on prostate cancer cell invasion and metastasis. Furthermore, in vitro growth and soft agar assays and in vivo growth experiments were performed to determine the function of DUSP6 in cell proliferation. The results showed that the overexpression of DUSP6 suppressed the invasion and growth of DU‑145 human prostate cancer cells, whereas knockdown of DUSP6 promoted the invasion and proliferation of LNCap human prostate adenocarcinoma cells. Further experiments demonstrated that the overexpression of DUSP6 inhibited the proliferation and liver metastasis of DU‑145 cells in mice. In addition, DUSP6 downregulated the expression of matrix metallopeptidase 3 and interleukin 8 in prostate cancer cells. Taken together, these findings indicate that DUSP6 may act as a negative mediator in the regulation of prostate cancer cell growth and metastasis.

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Crude extract of Euphorbia formosana inhibits the migration and invasion of DU145 human prostate cancer cells: The role of matrix metalloproteinase-2/9 inhibition via the MAPK signaling pathway

Cited by 13 publications

References 33 publications

Triticumoside induces apoptosis via caspase-dependent mitochondrial pathway and inhibits migration through downregulation of MMP2/9 in human lung cancer cells

Triticumoside induces apoptosis via caspase-dependent mitochondrial pathway and inhibits migration through downregulation of MMP2/9 in human lung cancer cells

Sulforaphane Inhibits Invasion via Activating ERK1/2 Signaling in Human Glioblastoma U87MG and U373MG Cells

Dual specificity phosphatase 6 suppresses the growth and metastasis of prostate cancer cells

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