吴乔
主要研究领域涉及肿瘤细胞生长抑制和细胞凋亡诱导的作用机理及信号转导调控;抗肿瘤药物抑制肿瘤生长、转移的分子机制;核受体蛋白相互作用和蛋白修饰等基础理论和应用研究。
个性化签名
- 姓名:吴乔
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学术头衔:
博士生导师, 国家杰出青年科学基金获得者
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学科领域:
细胞生物学
- 研究兴趣:主要研究领域涉及肿瘤细胞生长抑制和细胞凋亡诱导的作用机理及信号转导调控;抗肿瘤药物抑制肿瘤生长、转移的分子机制;核受体蛋白相互作用和蛋白修饰等基础理论和应用研究。
吴乔,女。1990年获得厦门大学理学硕士学位。在美国加州Burnham研究所完成博士论文研究工作后回国答辩,1996年获得厦门大学理学博士学位。
厦门大学生命科学学院教授,博士生导师,福建省“闽江学者”特聘教授。
目前主要研究领域涉及肿瘤细胞生长抑制和细胞凋亡诱导的作用机理及信号转导调控;抗肿瘤药物抑制肿瘤生长、转移的分子机制;核受体蛋白相互作用和蛋白修饰等基础理论和应用研究。
已在国际核心刊物如《The EMBO J.》、《Molecular and Cellular Biology》、《Journal of Cell Science》等和国内核心刊物如《中国科学》等发表论文40多篇。
获得国家杰出青年科学基金。近年来主持国家“973”重大项目预研基金、海外青年学者合作研究基金(合作主持)、国家自然科学基金(四项)、教育部重点科技项目、福建省自然科学基金(四项)等课题十多项。指导和培养博士生和硕士生20余名。
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吴乔, Qiao Wu, Yin Li, Ru Liu, Anissa Agadir, Mi-Ock Lee, Yi Liu and Xiao-kun Zhang
The EMBO Journal Vol. 16 No.7 pp. 1656-1669, 1997,-0001,():
-1年11月30日
The diverse function of retinoic acid (RA) is mediated by its nuclear receptors, the retinoic acid receptors (RARs) and retinoid X receptors (RXRs). However, the RA response is often lost in cancer cells that express the receptors. Previously, it was demonstrated that the RA response is regulated by the COUP-TF orphan receptors. Here, we present evidence that nur77, another orphan receptor whose expression is highly induced by phorbol esters and growth factors, is involved in modulation of the RA response. Expression of nur77 enhances ligand-independent transactivation of RA response elements (RAREs) and desensitizes demontheir RA responsiveness. Conversely, expression of COUP-TF sensitizes RA responsiveness of RAREs by repressing their basal transactivation activity. Unlike the effect of COUP-TFs, the function of nur77 does not require direct binding of nur77 to the RAREs, but is through interaction between nur77 and COUP-TFs. The interaction occurs in solution and results in inhibition of COUP-TF RARE binding and transcrip-tional activity. Unlike other nuclear receptors, a large portion of the carboxy-terminal end of nur77 is not required for its interaction with COUP-TF. In human lung cancer cell lines, COUP-TF is highly expressed in RA-sensitive cell lines while nur77 expression is associated with RA resistance. Stable expression of COUP-TF in nur77-positive, RA-resistant lung cancer RAcells enhances the inducibility of RARb gene expression and growth inhibition by RA. These observations predemonstrate that a dynamic equilibrium between orphan receptors nur77 and COUP-TF, through their heterodimerization that regulates COUP-TF RARE binding, is critical for RA responsiveness of human lung cancer cells.
lung cancer/, orphan receptors/, receptor dimerization/, retinoic acid receptors/, retinoic acid sensitivity
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吴乔, Qiao Wu, Su Liu, Xiao-feng Ye, Zhi-wei Huang and Wen-jin Su
Carcinogenesis vol. 23 no.10 pp. 1583-1592, 2002,-0001,():
-1年11月30日
Nur77 is an orphan receptor. Although Nur77 affects cell proliferation and apoptosis through its capability of binding to a variety of response elements and regulating their transactivation activities, the intrinsic function of Nur77 is not yet fully understood; in particular, its regulation of apoptosis and proliferation has been characterized as cell type-dependent and agent context-dependent. In this study, Nur77 can be seen to regulate apoptosis via its expression and translocation, rather than its transactivation activity in gastric cancer cells. Nur77 was constitutively expressed in BGC-823 cells. The tetradecanoylphorbol-1,3-acetate (TPA) treatment not only resulted in up-regulation of the Nur77 mRNA level, but also led to translocation of Nur77 protein from the nucleus to the mitochondria, and caused the release of cytochrome c. This TPA-induced translocation of Nur77 was in association with the initiation of apoptosis in gastric cancer cells. Although all-trans retinoic acid (ATRA) could not induce apoptosis in BGC-823 cells due to failure of stimulating Nur77 translocation, expression of Nur77 in the nucleus was required for cell growth inhibition by ATRA. Transfection of antisense Nur77 receptor into BGC-823 cells resulted in resistance of cell growth against ATRA inhibition, and the cells were still arrested in the S phase. Furthermore, the action of Nur77 in TPA-induced apoptosis was mediated through a protein kinase C signaling pathway, while mitogen-activated protein kinase and phosphatidylinositol 3-kinase signaling pathways were responsible for the regulation of Nur77 mRNA expression. Taken together, the data revealed the dual functioning mechanisms of Nur77 in gastric cancer cells in response to TPA and ATRA.
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吴乔, Xiao-Feng Lin*, Bi-Xing Zhao*, Hang-Zhi Chen, Xiao-Feng Ye, Chao-Yi Yang, Hai-Ying Zhou, Ming-Qing Zhang, Sheng-Cai Lin and Qiao Wu‡
Journal of Cell Science 117 (23), 5609-5621,-0001,():
-1年11月30日
Retinoid X receptor (RXR) plays a crucial role in the cross talk between retinoid receptors and other hormone receptors including the orphan receptor TR3, forming different heterodimers that transduce diverse steroid/thyroid hormone signaling. Here we show that RXRα exhibits nucleocytoplasmic shuttling in MGC80-3 gastric cancer cells and that RXRα shuttling is energydependent through a nuclear pore complex (NPC)-mediated pathway for its import and an intact DNA binding domain-mediated pathway for its export. In the presence of its ligand 9-cis retinoic acid, RXRα was almost exclusively located in the cytoplasm. More importantly, we also show that RXRα acts as a carrier to assist translocation of TR3, which plays an important role in apoptosis. Both RXRα and TR3 colocalized in the nucleus; however, upon stimulation by 9-cis retinoic acid they cotranslocated to the cytoplasm and then localized in the mitochondria. TR3 export depends on RXRα, as in living cells GFP-TR3 alone did not result in export from the nucleus even in the presence of 9-cis retinoic acid, whereas GFP-TR3 cotransfected with RXRα was exported out of the nucleus in response to 9-cis retinoic acid. Moreover, specific reduction of RXRα levels caused by anti-sense RXRα abolished TR3 nuclear export. In contrast, specific knockdown of TR3 by antisense-TR3 or TR3-siRNA did not affect RXRα shuttling. These results indicate that RXRα is responsible for TR3 nucleocytoplasmic translocation, which is facilitated by the RXRα ligand 9-cis retinoic acid. In addition, mitochondrial TR3, but not RXRα, was critical for apoptosis, as TR3 mutants that were distributed in the mitochondria induced apoptosis in the presence or absence of 9-cis retinoic acid. These data reveal a novel aspect of RXRα function, in which it acts as a carrier for nucleocytoplasmic translocation of orphan receptors.
Retinoid X receptor α (, RXRα), ,, Orphan receptor TR3,, 9-cis retinoic acid,, Nucleocytoplasmic translocation,, Gastric cancer cells
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