• Korean Journal of Environmental Biology
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• v.40 no.4
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• pp.525-549
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• 2022

The process of biological invasion is led by the dynamics of a population as a demographic and evolutionary unit. Spatial structure can affect the population dynamics, and it is worth being considered in research on biological invasion which is always accompanied by dispersal. Metapopulation theory is a representative approach to spatially structured populations, which is chiefly applied in the field of ecology and evolutionary biology despite the controversy about its definition. In this study, metapopulation was considered as a spatially structured population that includes at least one subpopulation with significant extinction probability. The early phase of the invasion is suitable to be analyzed in aspects of the metapopulation concept because the introduced population usually has a high extinction probability, and their ecological·genetic traits determining the invasiveness can be affected by the metapopulation structure. Although it is important in the explanation of the prediction of the invasion probability, the metapopulation concept is rarely used in ecological research about biological invasion in Korea. It is expected that applying the metapopulation theory can supply a more detailed investigation of the invasion process at the population level, which is relatively inadequate in Korea. In this study, a framework dividing the invasive metapopulation into long- and middle-distance scales by the relative distance of movement to the natural dispersal range of species is proposed to easily analyze the effect of a metapopulation in real cases. Increased understanding of the mechanisms underlying invasions and improved prediction of future invasion risk are expected with the metapopulation concept and this framework.

• BMB Reports
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• v.47 no.8
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• pp.445-450
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• 2014

Glucose regulated protein 78 (GRP78) is frequently highly expressed in tumor cells, contributing to the acquisition of several phenotypic cancer hallmarks. GRP78 expression is also positively correlated with tumor metastasis, and promotes hepatocellular carcinoma cell invasion via increasing cell motility, however, other mechanisms involving the prometastatic roles of GRP78 remain to be elucidated. Here we report that forced GRP78 expression promotes colon cancer cell migration and invasion through upregulating MMP-2, MMP-9 and especially uPA production. These effects of GRP78 are mediated by enhancing the activation of ${\beta}$-catenin signaling. Interestingly, we identify that GRP78 interacts with uPA both in the cells and in the culture medium, suggesting that GRP78 protein is likely to directly facilitate uPA secretion via protein-protein interaction. Taken together, our findings demonstrate for the first time that besides stimulation of cell motility, GRP78 can act by increasing proteases production to promote tumor cell invasion.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.9
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• pp.4815-4822
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• 2012

Invasion and metastasis are the major causes of cancer-related death. Pharmacological or therapeutic interventions such as chemoprevention of the progression stages of neoplastic development could result in substantial reduction in the incidence of cancer mortality. (-)-Epigallocatechin-3-gallate (EGCG), a promising chemopreventive agent, has attracted extensive interest for cancer therapy utilizing its antioxidant, anti-proliferative and inhibitory effects on angiogenesis and tumor cell invasion. In this study, we assessed the influence of EGCG on the proliferative potential of HeLa cells by cell viability assay and authenticated the results by nuclear morphological examination, DNA laddering assay and cell cycle analysis. Further we analyzed the anti-invasive properties of EGCG by wound migration assay and gene expression of MMP-9 and TIMP-1 in HeLa cells. Our results indicated that EGCG induced growth inhibition of HeLa cells in a dose- and time-dependent manner. It was observed that cell death mediated by EGCG was through apoptosis. Interestingly, EGCG effectively inhibited invasion and migration of HeLa cells and modulated the expression of related genes (MMP-9 and TIMP-1). These results indicate that EGCG may effectively suppress promotion and progression stages of cervical cancer development.

• Journal of Nutrition and Health
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• v.38 no.2
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• pp.104-111
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• 2005

Tumor invasion is composed of four steps: cell adhesion to the extracellular matrix, degradation of the extracellular matrix components, tumor cell motility followed by cell detachment. Matrix metalloproteinases (MMPs) are important proteinases that associated with degradation of matrix component. Epigallocatechin gallate (EGCG) is a major polyphenotic constituent of green tea. In the study, we examined the anti-invasive and MMP activity suppression effects of EGCG in MDA-MB-231 human breast cancer cells. MDA-MB-23l human breast cancer cells were cultured with various concentrations 0 - 100 μM of EGCG. EGCG significantly inhibited the cell adhesion to the fibronectin. Cell motility through gelatin filter and invasion to Matrigel were inhibited dose-dependently by EGCG treatment. EGCG also inhibited the activities of MMP-2, -9 and the amount of MMP-9 (α = 0.05). Therefore, EGCG may contribute to the potential beneficial food component to prevent the invasion and metastasis in breast cancer. (Korean J Nutrition 38(2): 104～111, 2005)

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.6
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• pp.2459-2463
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• 2015

Background: To investigate the expression and clinical significance of zinc finger protein 217 (ZNF217) in human colorectal carcinoma (CRC). Materials and Methods: The expression of ZNF217 in 60 CRC tissues and matched tumor adjacent tissues, collected between January 2013 and June 2014, was assessed immunohistochemically. The relationship between the expression of ZNF217 and clinicopathlogical features was analyzed by Pearson chi-square test. In addition, siRNA was used to down-regulate the expression of ZNF217 in CRC cells. The effects of ZNF217 for cell migration and invasion were measured by wound healing assay and transwell assay, respectively. Results: The expression level of ZNF217 was significantly higher in CRC tissues than in tumor adjacent tissues (p<0.05), positively correlating with tumor size, lymphatic metastasis and advanced TNM stage (p<0.05). Down-regulation of ZNF217 in CRC cells could significantly suppress cell migration and invasion. Conclusions: ZNF217 is overexpressed in colorectal carcinoma tissues and is associated with tumor malignant clinicopathological features. ZNF217 may promote CRC progression by inducing cell migration and invasion.

• Nutrition Research and Practice
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• v.5 no.5
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• pp.375-380
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• 2011

This study investigated the effects of inorganic sulfur on metastasis in MDA-MB-231 human breast cancer cells. MDA-MB-231 cells were cultured in the absence or presence of various concentrations (12.5, 25, or 50 ${\mu}mol$/L) of inorganic sulfur. Cell motility, invasion, and the activity and mRNA expression of matrix metalloproteases (MMPs) were examined. Numbers of viable MDA-MB-231 cells did not differ by inorganic sulfur treatment from 0 to 50 ${\mu}mol$/L within 48 h. Inorganic sulfur significantly decreased cell motility and invasion in the MDA-MB-231 cells in a dose-dependent manner (P<0.05), as determined using a Boyden chamber assay and a Matrigel chamber. The activities of MMP-2 and MMP-9 were significantly reduced by inorganic sulfur in a dose-dependent manner (P<0.05). The inorganic sulfur also significantly inhibited MMP-2 and MMP-9 expression in the cells (P<0.05). These data suggest that inorganic sulfur can suppress cancer cell motility and invasion by inhibiting MMP-2 and MMP-9 activity and gene expression in MDA-MB-231 cells.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.4
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• pp.1097-1104
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• 2012

Background/Aim: Pristimerin isolated from Celastrus and Maytenus spp can inhibit proteasome activity. However, whether pristimerin can modulate cancer metastasis is unknown. Methods: The impacts of pristimerin on the purified and intracellular chymotrypsin proteasomal activity, the levels of regulator of G protein signaling 4 (RGS 4) expression and breast cancer cell lamellipodia formation, and the migration and invasion were determined by enzymatic, Western blot, immunofluorescent, and transwell assays, respectively. Results: We found that pristimerin inhibited human chymotrypsin proteasomal activity in MDA-MB-231 cells in a dose-dependent manner. Pristimerin also inhibited breast cancer cell lamellipodia formation, migration, and invasion in vitro by up-regulating RGS4 expression. Thus, knockdown of RGS4 attenuated pristimerin-mediated inhibition of breast cancer cell migration and invasion. Furthermore, pristimerin inhibited growth and invasion of implanted breast tumors in mice. Conclusion: Pristmerin inhibits proteasomal activity and increases the levels of RGS4, inhibiting the migration and invasion of breast cancer cells.

• THE JOURNAL OF KOREAN ORIENTAL ONCOLOGY
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• v.7 no.1
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• pp.109-116
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• 2001

By applying in vitro invasion assay model, we examined the anti-metatstastic effect of ChunghjagamTang(CLJGT). In 3H-thymidine incorporation assay, CLJGT treated groups showed the decreased DNA synthesis rate compared with control group. Gelatin zymogram assay showed that CLJGT decreases the gelatinolytic activity of MMP-9 from A-549, at the concentration of $800{\mu}g/ml$. We examined whether CLJGT inhibits the invasion of A-549 cells through the matrigel precoated transwell chamber. The results showed that CLJGT effectively inhibited the invasion of A-549 as compared with the control (+PMA) groups. From our research, part of mechanism underlying anti-metastastic effect of CLJGT was proven in vitro.

• Toxicological Research
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• v.23 no.3
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• pp.197-205
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• 2007

Cancer metastasis is a major determinant of cancer patient mortality. Mounting evidence favors a strong positive role for $TGF-{\beta}$ in human cancer progression. The complex pattern on cross-talk of $TGF-{\beta}$ and the related other signaling pathways is an important area of investigation that will ultimately contribute to understanding of the bifunctional role of $TGF-{\beta}$ in cancer progression. This review summarizes some of the current understanding of $TGF-{\beta}$ signaling with a major focus in its contribution to the tumor cell invasion and metastasis. Five issues are addressed in this review: (1) $TGF-{\beta}$ signaling, (2) $TGF-{\beta}$ and EMT, (3) $TGF-{\beta}$ and MMP, (4) $TGF-{\beta}$ and Ras, and (5) Role of $TGF-{\beta}$ in invasion and metastasis. Due to the bifunctional cellular effects of $TGF-{\beta}$, as a tumor promoter and a tumor suppressor, more precisely defined $TGF-{\beta}$ signaling pathways need to be elucidated. According to the current literature, $TGF-{\beta}$ is clearly a major factor stimulating tumor progression through a complex spectrum of the interplay and cross-talk between various signaling molecules. Understanding the role of $TGF-{\beta}$ in invasion and metastasis will provide valuable information on establishing strategies to manipulate $TGF-{\beta}$ signaling which should be a high priority for the development of anti-metastatic therapeutics.

• BMB Reports
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• v.48 no.10
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• pp.559-564
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• 2015

We investigated the effects of mangiferin on the expression and activity of metalloproteinase (MMP)-9 and the invasion of tumor necrosis factor (TNF)-$\alpha$-stimulated human LNCaP prostate carcinoma cells. Reverse-transcription polymerase chain reaction (RT-PCR) and western blot analysis showed that mangiferin significantly reversed TNF-$\alpha$-induced mRNA and protein expression of MMP-9 expression. Zymography data confirmed that stimulation of cells with TNF-$\alpha$ significantly increased MMP-9 activity. However, mangiferin substantially reduced the TNF-$\alpha$-induced activity of MMP-9. Additionally, a matrigel invasion assay showed that mangiferin significantly reduced TNF-$\alpha$-induced invasion of LNCaP cells. Compared to untreated controls, TNF-$\alpha$-stimulated LNCaP cells showed a significant increase in nuclear factor-${\kappa}B$ (NF-${\kappa}B$) luciferase activity. However, mangiferin treatment markedly decreased TNF-$\alpha$-induced NF-${\kappa}B$ luciferase activity. Furthermore, mangiferin suppressed nuclear translocation of the NF-${\kappa}B$ subunits p65 and p50. Collectively, our results indicate that mangiferin is a potential anti-invasive agent that acts by suppressing NF-${\kappa}B$-mediated MMP-9 expression.