• Asian Pacific Journal of Cancer Prevention
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• v.15 no.20
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• pp.8829-8836
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• 2014

Background: Cyclooxygenase-2 (COX-2), considered to have tumor-promoting potential, is highly expressed in a variety of tumors, including breast cancer. Since the functions and action mechanisms of COX-2 in breast cancer have not been fully elucidated, in the present study, the effects of target inhibiting COX-2 with recombinant adenovirus Ad-COX-2-shRNA on malignant biological behavior were investigated in representative cell lines. Materials and Methods: Breast cancer MDA-MB-231 and MCF-7 cells were transfected with Ad-COX-2-shRNA and COX-2 expression was tested by RT-PCR and Western blotting. Changes in proliferation, apoptosis and invasion of breast cancer cells were detected with various assays including MTT, colony forming, flowcytometry and Transwell invasion tests. The expression of related proteins involved in the cell cycle, apoptosis, invasion and signaling pathways was assessed by Western blotting. Results: COX-2 expression was significantly reduced in both breast cancer cell lines infected with Ad-COX-2-shRNA, with obvious inhibition of proliferation, colony forming rate, G2/M phase passage and invasion, as well as induction of apoptosis, in MDA-MB-231 and MCF-7 cells, respectively. At the same time, proteins related to the cell cycle, anti-apoptosis and invasion were significantly downregulated. In addition, c-myc expression and phosphorylation activation of Wnt/${\beta}$-catenin and p38MAPK pathways were reduced by the Ad-COX-2-shRNA. Conclusions: COX-2 expression is associated with proliferation, apoptosis and invasion of breast cancer cells, and its mechanisms of action involve regulating expression of c-myc through the p38MAPK and Wnt/${\beta}$-catenin pathways.

• Journal of Ginseng Research
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• v.34 no.2
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• pp.138-144
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• 2010

Ginseng (Panax ginseng C.A. Meyer) has been shown to have anti-stress effects in animal studies. However, most studies have only managed to detect altered levels of biomarkers or enzymes in blood or tissue, and the actual molecular mechanisms by which ginseng exerts these effects remain unknown. In this study, the anti-oxidative effect of Korean red ginseng (KRG) was examined in human SK-N-SH neuroblastoma cells. Incubation of SK-N-SH cells with the oxidative stressor hydrogen peroxide resulted in significant induction of cell death. In contrast, pre-treatment of cells with KRG decreased cell death significantly. To elucidate underlying mechanisms by which KRG inhibited cell death, the expression of apoptosis-related proteins was examined by Western blot analysis. KRG pre-treatment decreased the expression of the pro-apoptotic gene caspase-3, whereas it increased expression of the anti-apoptotic gene Bcl-2. Consistent with this, immunoblot analysis showed that pre-treatment of the SK-N-SH cells with KRG inhibited expression of the pro-inflammatory gene cyclooxygenase 2 (COX-2). RT-PCR analysis revealed that the repression of COX-2 expression by KRG pre-treatment occurred at the mRNA level. Taken together, our data indicate that KRG can protect against oxidative stress-induced neuronal cell death by repressing genes that mediate apoptosis and inflammation.

• Journal of Life Science
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• v.34 no.8
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• pp.558-566
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• 2024

The potential therapeutic effects of Kaempferia Parviflora ethanol extract (KPE) on osteoarthritis were investigated using the human chondrocyte cell line (CHON-001) to explore its application in functional foods. The CHON-001 cells were pre-treated with either 1 ㎍/ml or 5 ㎍/ml of KPE before exposure to 10 ng/ml of IL-1β to induce osteoarthritis. Results showed that KPE treatment significantly suppressed IL-1β-induced TNF-α production by 66% and 50% at concentrations of 1 ㎍/ml and 5 ㎍/ml KPE, respectively. In addition, COX-2 protein expression was reduced by 26% and 34% compared to control levels. The preservation of chondrocyte-specific matrix proteins, aggrecan, and collagen type II, was notable, with aggrecan and mRNA levels maintained by 5% and 8%, and collagen II levels preserved by 62% and 47% at the same KPE concentrations. This preservation is likely due to the reduced expression of MMP1 and MMP13, enzymes responsible for matrix protein degradation. Overall, the current results suggest that KPE may protect chondrocytes from IL-1β-induced osteoarthritis by suppressing TNF-α production and COX-2 expression while preserving critical matrix proteins like aggrecan and collagen II by suppressing the expressions of their degrading enzymes (MMP-1 and MMP-13). Therefore, KPE holds promise as a candidate for developing functional foods aimed at reducing osteoarthritis.