曹亚
个性化签名
- 姓名:曹亚
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学术头衔:
博士生导师
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学科领域:
病理学
- 研究兴趣:
曹亚,女,博士生导师、病理与病理生理学国家重点学科学术带头人,湘雅医学院副院长、肿瘤研究所副所长,卫生部癌变原理重点实验室及教育部癌变与侵袭重点实验室副主任。第五届国务院学位委员会委员,第八、九届国家自然科学基金、973项目以及科技部国家自然科学奖评审专家,中华医学会病理生理学会肿瘤专业委员会主任委员。 1985至今先后五次获得国际抗癌联盟及美国洛克非勒基金的资助,赴美国国立癌症研究院作高级访问学者。回国后主要成就如下:(1)主持973项目、国家杰出青年基金、国家自然科学基金重点及面上项目、CMB及省部级课题20余项;(2)获国家科技进步二等奖、 卫生部科技进步二等奖、湖南医学科技一等奖;(3)获国家“做出突出贡献的中国硕士学位获得者”、 “突出贡献的中青年专家”、湖南省“跨世纪学术带头人”及“优秀留学回国人员”。(4)已培养研究生22名,在读14名。(5)发表学术论文100余篇,主编专著1部。
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2362
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成果阅读
217
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成果数
5
曹亚, Ming Li, De-yun Feng, Wei Ren, Liang Zheng, Hui Zheng, Min Tang, Ya Cao*
The International Journal of Biochemistry & Cell Biology xxx(2004)xxx-xxx,-0001,():
-1年11月30日
Although it is generally believed that, under normal conditions, the only source ofimmunoglobulin is mature B lymphocytes, we recently found several epithelium-derived carcinoma cell lines also express immunolglobulin-like protein. We extended our study to biopsy samples of human cervical tissues with various epithelial lesions. By in situ hybridization, we only detected a low level ofmRNA for the immunoglobulin kappa light chain constant region in epithelia with cervicitis. However, in epithelia with dysplasia and carcinoma, the expression of mRNA for the kappa constant region was markedly increased. There was no significant difference in the level of mRNA for the kappa constant region between epithelial dysplasia and carcinoma. The aberrant expression ofimmunoglobulin kappa light chain constant region in dysplastic and cancerous cervical epithelial cells may serve as a marker for malignant cell transformation.
Ig kappa light chain, Epithelial carcinoma, B lymphocyte, In situ hybridization, Cervical tissue
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曹亚, Zhao Yan, Tao Yong-Guang, Luo Fei-Jun, Tang Fa-Qing, Tang Min, Cao Ya*
,-0001,():
-1年11月30日
Aim: To elucidate the interference effect of epigallocatechin-3-gallate (EGCG) on targets of nuclear factor _B (NF-_B) signal transduction pathway activated by EB virus encoded latent membrane protein 1 (LMP1) in nasopharyngeal carcinoma (NPC) cell lines. Methods: The survival rates of CNE1 and CNE-LMP1 cell lines after the EGCG treatment were determined by MTT assay. NF-_B activation in CNE1 and CNE-LMP1 cells after EGCG treatment was analyzed by promoter luciferase reporter system. And then nuclear translocation of NF-_B (p65) after the EGCG treatment was analyzed by immunofluorescence and western blotting. Meanwhile, the changes of I_B_ phosphorylation were observed after the EGCG treatment. EGFR promoter activity was analyzed by promoter luciferase reporter system and EGFR phosphorylation was observed by western blotting after the EGCG treatment. Results: EGCG inhibited the survival rates of CNE1 and CNE-LMP1 cells and NF-_B activation caused by LMP1 in CNE-LMP1 cells. EGCG also suppressed the nuclear translocation of NF-_B (p65) and I_B_ phosphorylation. Meanwhile, EGCG inhibited EGFR promoter activity and EGFR phosphorylation. Conclusions: EGCG inhibited not only the dose-dependent survival rate of NPC cells, but also the dose-dependent activation of NF-_B. This inhibition of LMP1-caused NF-_B activation was mediated via the phosphorylative degradation of its inhibitory protein I_B_, and then EGCG inhibited EGFR activity which was a downstream gene from NF-_B. This study suggests that interference effect of EGCG on targets of signal transduction pathway plays an important role in the anticancer function.
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曹亚, Yong-guang Tao, Yun-nian Tan, Yi-ping Liu, Xin Song, Liang Zeng, Huang-hua Gu, Ming Tang, Wei Li, Wei Yi, Ya Cao*
,-0001,():
-1年11月30日
The Epstein-Barr virus (EBV) latent membrane protein 1 (LMP1) oncoprotein may cause multiple cellular changes including the induction of epidermal growth factor receptor (EGFR) expression and activation of the NFnB transcription factor. LMP1 increases the levels of both EGFR protein and mRNA, but does not stabilize EGFR mRNA. Thus, the effects of LMP1 are likely to be mediated by the direct activation of the EGFR promoter. In this study, induction of LMP1 increased the EGFR in both protein and promoter levels in a dosedependent manner using tetracycline-regulated LMP1 expression in nasopharyngeal carcinoma (NPC) cell line. Mutational analysis of the LMP1 protein indicated that the C-terminal activation region-1 (CTAR1) domain was mainly involved in the EGFR promoter induction, while CTAR2 was necessary but not sufficient to induce EGFR promoter. Inhibition of LMP1-mediated NFnB activation by constitutive repressive InBa marginally decreased EGFR promoter activity using transiently transfected InBa dominant negative mutant. Promoter mutagenesis analysis demonstrated that two putative NFnB binding sites of EGFR promoter were very necessary for the transcriptional activity of EGFR induced by LMP1, the proximal NFnB binding site was more important than the distal NFnB binding site, and both NFnB binding sites played a cooperative role. Taken together, Epstein-Barr virus latent membrane protein 1 modulated the EGFR promoter activity in a NFnB-dependent manner.
Latent membrane protein 1, Epidermal growth factor receptor, Promoter, Nuclear factor kappa B, Nasopharyngeal carcinoma, Epstein-Barr virus, Inhibitory kappa B alpha, C-terminal activation region-1 (, CTAR1), , CTAR2, Tetracycline
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曹亚, Xin Songa, Yong-Guang Taoa, Xi-Yun Denga, Xin Jina, Yun-Nian Tana, Min Tanga, Qiao Wub, Leo M. Leec, Ya Caoa, *
,-0001,():
-1年11月30日
Epstein-Barr virus (EBV) encoded latent membrane protein 1 (LMP1) is essential for the mmortalization of human B cells and is linked etiologically to several human tumors. LMP1 is an integral membrane protein which acts like a constitutively active receptor. It binds tumor necrosis factor (TNF)-receptor-associated factors (TRAFs), activates NFnB and triggers the transcription factor activating protein-1 (AP-1) via the c-Jun N-terminal kinase (JNK) cascade, but its specific contribution to AP-1 has not been elucidated fully. Members of AP-1 family, the Jun and fos related protein, have been shown to directly interact and form heterodimeric complexes. In this report, using a Tet-on LMP1 HNE2 cell line which is a dual-stable LMP1 integrated nasopharyngeal carcinoma (NPC) cell line and the expression of LMP1 in which could be regulated by Tet-on system, we show that Jun B can efficiently form a new heterodimeric complex with the c-Jun protein under the regulation of LMP1, phosphorylation of c-Jun (ser63, ser73) and Jun B involved in the process of the new heterodimeric form. We also find that this heterodimeric form can bind to the AP-1 consensus sequence. Transfection studies suggest that JNK interaction protein (JIP) could inhibit the heterodimer form of c-Jun and Jun B through blocking the AP-1 signaling pathway triggered by LMP1. The interaction and function between c-Jun protein and Jun B protein increase the repertoire of possible regulatory complexes by LMP1 that could play an important role in the regulation of transcription of specific cellular genes in the process of genesis of nasopharyngeal carcinoma.
Epstein-Barr virus, Latent membrane protein 1, Jun B, c-Jun, Heterodimer, DNA binding, JNK, JIP
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曹亚, Yong-guang Tao, Yun-nian Tan, Yi-ping Liu, Xin Song, Liang Zeng, Huang-hua Gu, Ming Tang, Wei Li, Wei Yi, Ya Cao*
,-0001,():
-1年11月30日
and mRNA but does not stabilize EGFR mRNA. Thus the effects of LMP1 are likely to be mediated by direct activation of the EGFR promoter. In this study, induction of LMP1 increased the EGFR in both protein and promoter levels in a dose dependent manner using tetracycline-regulated LMP1 expression in nasopharyngeal carcinoma (NPC) cell line. Mutational analysis of the LMP1 protein indicated that the C-terminal activation region-1 (CTAR1) domain was mainly involved in the EGFR promoter induction, while CTAR2 was necessary but not sufficient to induce EGFR promoter. Inhibition of LMP1 mediated NF_B activation by constitutive repressive inhibitory kappa B alpha (I_B_) marginally decreased EGFR promoter activity using transiently transfected I_B_ dominant negative mutant. Promoter mutagenesis analysis demonstrated that two putative NF_B binding sites of EGFR promoter were very necessary for the transcriptional activity of EGFR induced by LMP1, the proximal NF_B binding site was more important than the distal NF_B binding site. Taken together, Epstein–Barr virus latent membrane protein 1 modulated the EGFR promoter activity in a NF_B dependent manner.
Latent membrane protein 1, Epidermal growth factor receptor, Promoter, Nuclear factor kappa B, Nasopharyngeal carcinoma, Epstein-Barr virus, Inhibitory kappa B alpha, C-terminal activation region-1 (, CTAR1), , CTAR2, Tetracycline
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