• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2003.10a
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• pp.142-142
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• 2003

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2001.10b
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• pp.133-134
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• 2001

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2002.05a
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• pp.80-80
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• 2002

• Proceedings of the PSK Conference
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• 2000.10a
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• pp.197.3-198
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• 2000

• Proceedings of the Korean Society of Toxicology Conference
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• 2001.10a
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• pp.156-156
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• 2001

We have previously shown that H-ras, but N-ras, induces an invasiveness and cell motility in human breast epithelial cells (MCFl0A), while both H-ras and N-ras induce transformed phenotype. It has been recently shown that phosphatidylinositol 3-kinase (PI3K) plays an important role on cell migration. In the present study, we wished to investigate the functional role of PI3K in H-ras-induced invasive phenotype in MCF10A cells.(omitted)

• International Journal of Oral Biology
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• v.45 no.4
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• pp.152-161
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• 2020

D-pinitol is an analog of 3-methoxy-D-chiro-inositol found in beans and plants. D-pinitol has anti-inflammatory, antidiabetic, and anticancer effects. Additionally, D-pinitol induces apoptosis and inhibits metastasis in breast and prostate cancers. However, to date, no study has investigated the anticancer effects of D-pinitol in oral cancer. Therefore, in this study, whether the anticancer effects of D-pinitol induce apoptosis, inhibit the epithelial-to-mesenchymal transition (EMT), and arrest cell cycle was investigated in squamous epithelial cells. D-pinitol decreased the survival and cell proliferation rates of CAL-27 and Ca9-22 oral squamous carcinoma cells in a concentration- and time-dependent manner. Evidence of apoptosis, including nuclear condensation, poly (ADP-ribose) polymerase, and caspase-3 fragmentation, was also observed. D-pinitol inhibited the migration and invasion of both cell lines. In terms of EMT-related proteins, E-cadherin was increased, whereas N-cadherin, Snail, and Slug were decreased. D-pinitol also decreased the expression of cyclin D1, a protein involved in the cell cycle, but increased the expression of p21, a cyclin-dependent kinase inhibitor. Hence, D-pinitol induces apoptosis and cell cycle arrest in CAL-27 and Ca9-22 cells, demonstrating an anticancer effect by decreasing the EMT.

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.05a
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• pp.89-90
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• 2003

Extracts of Artemisia asiatica Nakai (Asteraceae) have been shown to have anti-inflammatory and anti-oxidative activities. Eupatilin (5,7-dihydroxy-3,4,6-tri-methoxy-flavone), one of the pharmacologically active ingredients derived from Artemisia asiatica, has been shown to induce apoptosis in promyelocytic leukemia (HL-60) cells. (omitted)

• Proceedings of the Korean Society of Toxicology Conference
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• 2001.10a
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• pp.133-134
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• 2001

Abnormal regulation of the inducible form of cyclooxygenase (COX-2) has been often observed in various types of cancerous and transformed cells. Recently, targeted inhibition of COX-2 is recognized as one of the promising strategies for the prevention or treatment of cancer as well as inflammation, As part of a program to evaluate the cancer chemopreventive potential of anti-inflammatory phytochemicals, we initially determined the COX-2 inhibitory activity of some naturally occurring diarylheptanoids structurally related to curcumin.(omitted)

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.223.1-223.1
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• 2003

Many studies have identified the phosphatidylinositol 3-kinase (PI3K) as a key regulator for various cellular functions including cell survival, growth and motility. We have previously shown that H-ras, but not N-ras. induces invasiveness and motility in human breast epithelial cells (MCF10A), while both H-ras and N-ras induce transformed phenotype. In the present study, we wished to investigate the functional role of PI3K pathway in H-ra-induced invasive phenotype and motility of MCF10A cells. (omitted)

• Korean Journal of Clinical Laboratory Science
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• v.55 no.1
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• pp.37-44
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• 2023

Enterotoxigenic Bacteroides fragilis (ETBF) has been reported to promote colitis and colon cancer through the secretion of B. fragilis toxin (BFT), a zinc-dependent metalloprotease. In colonic epithelial cells, BFT induces the cleavage of E-cadherin into the 80 kDa ectodomain and the 33 kDa membrane-bound intracellular domain. The resulting membrane-tethered fragment is then cleaved by γ-secretase forming the 28 kDa E-cadherin intracellular fragment. The 28 kDa cytoplasmic fragment is then degraded by an unknown mechanism. In this study, we found that the 28 kDa E-cadherin intracellular fragment was degraded by the proteasome complex. In addition, we found that this sequential E-cadherin cleavage mechanism is found not only in colonic epithelial cells but also in the human breast cancer cell line, BT-474. Finally, we report that staurosporine also induces E-cadherin cleavage in the human breast cancer cell line, MCF7, through γ-secretase. However, further degradation of the 28 kDa E-cadherin intracellular domain is not dependent on the proteasome complex. These results suggest that the BFT-induced E-cadherin cleavage mechanism is conserved in both colonic and breast cancer cells. This observation indicates that ETBF may also play a role in the carcinogenesis of tissues other than the colon.