Novel Molecular Target for Breast Cancer Prevention and Treatment

机译：一种新的乳腺癌预防和治疗分子靶点

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We have investigated the mechanism by which retinoids induce apoptosis in breast cancer cells. Our results reveal a new apoptosis paradigm involving translocation of orphan receptor TR3 from the nucleus to the cytoplasm, where it targets mitochondria to induce cytochrome c release and apoptosis. The translocation of TR3 requires its unique heterodimerization with retinoid X receptor (RXRalpha). A putative nuclear export sequence (NES) in RXRalpha mediates nuclear export of TR3/RxRalpha heterodimer. The RXRalpha NES activities are regulated by RXRX dimerization and ligand-binding. In studying how TR3 targets mitochondria, we have discovered that TR3 targets mitochondria through its interaction with Bcl-2. Bcl-2 acts as a mitochondrial receptor of TR3. It mediates the pro-apoptotic effects of TR3 by undergoing a conformational change upon TR3 binding. Such a conformational change converts Bcl-2 from a protector to killer. Together, our studies reveal a novel apoptotic pathway involving TR3, RXRalpha and Bcl-2 in breast cancer cells and our results provide various new strategies for developing agents against breast cancer.

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作者
Zhang, X.;
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年度 2004
页码 1-108
总页数 108
原文格式 PDF
正文语种 eng
中图分类工业技术;
关键词
Membranes(Biology); Preventive medicine; Mitochondria; Breast cancer; Apoptosis; Molecules; Targets; Therapy; Cytoplasm; Targeting; Cells(Biology); Vitamin a; Nuclei(Biology);

机译：膜（生物学）;预防医学;线粒体;乳腺癌;细胞凋亡;分子;靶点;治疗;细胞质;靶向;细胞（生物学）;维生素a;细胞核（生物学）;

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Novel Molecular Target for Breast Cancer Prevention and Treatment

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