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Mutant p53-Notch1 Signaling Axis Is Involved in Curcumin-Induced Apoptosis of Breast Cancer Cells
배윤희,류종효,박현주,위희준,이옥희,장혜옥,배문경,김규원,배수경,김광록 대한약리학회 2013 The Korean Journal of Physiology & Pharmacology Vol.17 No.4
Notch1 has been reported to be highly expressed in triple-negative and other subtypes of breast cancer. Mutant p53 (R280K) is overexpressed in MDA-MB-231 triple-negative human breast cancer cells. The present study aimed to determine whether the mutant p53 can be a potent transcriptional activator of the Notch1 in MDA-MB-231 cells, and explore the role of this mutant p53-Notch1 axis in curcumin-induced apoptosis. We found that curcumin treatment resulted in an induction of apoptosis in MDA-MB-231 cells, together with downregulation of Notch1 and its downstream target, Hes1. This reduction in Notch1 expression was determined to be due to the decreased activity of endogenous mutant p53. We confirmed the suppressive effect of curcumin on Notch1 transcription by performing a Notch1 promoter-driven reporter assay and identified a putative p53-binding site in the Notch1promoter by EMSA and chromatin immunoprecipitation analysis. Overexpression of mutant p53increased Notch1 promoter activity, whereas knockdown of mutant p53 by small interfering RNA suppressed Notch1 expression, leading to the induction of cellular apoptosis. Moreover, curcumin-induced apoptosis was further enhanced by the knockdown of Notch1 or mutant p53, but it was decreased by the overexpression of active Notch1. Taken together, our results demonstrate, for the first time, that Notch1 is a transcriptional target of mutant p53 in breast cancer cells and suggest that the targeting of mutant p53 and/or Notch1 may be combined with a chemotherapeutic strategy to improve the response of breast cancer cells to curcumin.
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백선용,김수련,황지원,배문경,위희준,최영현,오세옥,김봉선,윤식,배수경,김재봉 대한암예방학회 2006 Journal of cancer prevention Vol.11 No.3
Trichostatin A (TSA) shows a promising therapeutic effect on cancer cells when combined with radiotherapy or chemotherapy. However, so far, little has been reported on the combined treatment with TSA and hyperthermia (heat shock: HS). Here, we examined the effect of TSA/HS on human astrocytoma A172 cells and found that TSA/HS cotreatment effectively induced apoptotic cell death. The molecular mechanism of this effect consists of reduction in the levels of antiapoptotic factors (Bcl-2 and XIAP), Hsp27, and phosphorylated STAT3 (Tyr705), a transcription factor required for survival of A172 cells. Reduction of STAT3 activity resulted in the down-regulation of its taget genes, Bcl-xL and VEGF. In contrast, the level of p53 tumor suppressor was increased by TSA/HS. Therefore, our results show that co-treatment of TSA and HS play a role as an effective inducer of apoptosis in STAT3- dependent tumor cells such as A172 cells. (Cancer Prev Res 11, 205-210, 2006)
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박선영(Seon-Yeong Park),강용규(Yong-Gyu Kang),배윤희(Yun-Hee Bae),김수륜(Su-Ryun Kim),박현주(Hyun-Joo Park),강영순(Young-Soon Kang),김미경(Mi-Kyoung Kim),위희준(Hee-Jun Wee),장혜옥(Hye-Ock Jang),배문경(Moon-Kyoung Bae),우재석(Jae Suk 한국생물공학회 2013 KSBB Journal Vol.28 No.1
Curcumin has diverse anticancer activities that lead to tumor growth inhibition of cancer cells and induction of apoptosis. Curcumin is involved in the regulation of multiple genes via transcription factors including NF-kB, STATs, AP1, and SP. Notch signaling plays critical roles in maintaining the balance between cell proliferation, differentiation and apoptosis, and thereby may contribute to the development of various cancers involving breast cancer. This study was to investigate the effects of curcumin on Notch1 gene expression and to explore the underlying mechanism. Here, we found that curcumin decreased the levels of Notch1 mRNA and protein in MDA-MB-231 human breast cancer cells, along with the downregulation of Sp family genes (Sp1, Sp2, Sp3, and Sp4). The repressive effect of curcumin on Notch1 gene transcription was confirmed by performing Notch1 promoter- driven reporter assay and three Sp-binding sites were identified on Notch1 promoter that may act as curcumin-respose elements. Moreover, treatment with mitramycin A, a specific Sp inhibitor, decreased the levels of Notch1 mRNA and protein in human breast cancer cells. Taken together, our results indicate that Notch1 gene expression is downregulated by curcumin, at least in part, through the suppression of Sp family, which may lead to apoptosis in human breast cancer cells.
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