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RISS 인기검색어
- 검색키워드
- 저자 : ( Mi Kyoung Kwa ) (검색결과 2 건)
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( Mi Yeon Cho ),( Su Young Park ),( Su Min Park ),( Yong Rok Lee ),( Mi Kyoung Kwa ),( Jung Ae Kim ) 영남대학교 약품개발연구소 2012 영남대학교 약품개발연구소 연구업적집 Vol.22 No.0
Polyphenols are known to induce apoptosis in many cancer cells and are proposed to be promising modulators of drug resistance. In the present study, we report that 3-geranyl-phloroacetophenone (3-GAP), a synthetic polyphenol, induces apoptosis and modulates drug resistance. In adriamycin-resistant MCF-7 human breast cancer (MCF-7/ADR) cells, which express a mutant form of p53, 3-GAP induced significant apoptosis, which was accompanied by no change in p53 transcriptional activity, but an increase in Bax expression, cyt c release, and activation of caspase-9, 7, and 3. In addition, 3-GAP significantly decreased the activity and expression level of glutathione S-transferase pi (GSTπ), a factor that induces drug resistance. Along with GSTπ inhibition, 3-GAP also induced a marked depletion of GSH, an endogenous antioxidant. The GST-inhibitory activity of 3-GAP correlated with the sensitization of MCF-7/ADR cells to doxorubicin. Under serum withdrawal conditions, the JNK inhibitor SP600125 significantly decreased the viability of the parent MCF-7 cells but not of MCF-7/ADR cells. In addition, the viability of 3-GAP-treated MCF-7/ADR cells was similar to those of MCF-7 cells treated with SP600125 alone or MCF-7/ADR cells co-treated with SP600125 and 3-GAP. These results indicate that JNK activity in MCF-7/ADR cells is halted by high levels of GSTπ, and that 3-GAP releases JNK from GSTπ`s inhibition. In conclusion, 3-GAP induces apoptosis in and sensitizes drug-resistant MCF-7/ADR cells. These effects are mediated through p53-independent caspase-3 activation and reduction of the capacity for cellular antioxidants, such as GSTπ and GSH.
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( Sarala Manandhar ),( Bo Hyun Choi ),( Kyeong Ah Jung ),( In Geun Ryoo ),( Min Gu Song ),( Su Jin Kang ),( Han Gon Choi ),( Jung Ae Kim ),( Pil Hoon Park ),( Mi Kyoung Kwa ) 영남대학교 약품개발연구소 2012 영남대학교 약품개발연구소 연구업적집 Vol.22 No.0
NF-E2-related factor 2 (NRF2) is a transcription factor that regulates the expression of various antioxidant and detoxifying enzymes. Although the benefit of NRF2 in cancer prevention is well established, its role in cancer pathobiology was recently discovered. In this study, the role of NRF2 in tumor growth and docetaxel sensitivity was investigated in ErbB2-overexpressing ovarian carcinomaSKOV3 cells. Interfering RNA-mediated stable inhibition of NRF2 in SKOV3 cells repressed NRF2signaling, resulting in cell growth arrest at G(0)/G(1) phase and tumor growth retardation in mouse xenografts. Microarray analysis revealed that ErbB2 expression is substantially reduced in NRF2-inhibited SKOV3 and this was further confirmed by RT-PCR and immunoblot analysis. Repression ofErbB2 led to a decrease in phospho-AKT and enhanced p27 protein, reinforcing the effect of NRF2knockdown on SKOV3 growth. Furthermore, NRF2 inhibition-mediated ErbB2 repression increases the sensitivity of these cells to docetaxel cytotoxicity and apoptosis. The linkage between NRF2 andErbB2 was confirmed in the ErbB2-positive breast cancer cell line BT-474: NRF2 knockdown suppressed ErbB2 expression and enhanced docetaxel sensitivity. Our results provide insight into the coordinated regulation of signaling molecules responding to environmental stress and suggest thatNRF2 modulation might be a therapeutic strategy to limit tumor growth and enhance sensitivity to taxane-based chemotherapy. ⓒ 2012 Elsevier Lnc. All rights reserved.
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