加拿大研究人员发现了一种能够调节细胞凋亡机制的蛋白质，该新发现对癌症的诊断和治疗都将产生影响。此项研究成果发表在《分子癌症研究》杂志的网络版上。
该项目研究人员、西安大略大学罗伯兹癌症研究所的卡罗琳·席尔德-保尔特解释道，鉴别出的蛋白质RanBPM可直接参与激活细胞凋亡。癌症的主要特点之一是，细胞尽管在其遗传物质中有缺陷，但细胞并不主动凋亡。换句话说，受损细胞不能确保会自杀，从而发展成癌症。无法激活细胞凋亡也造成了癌症治疗的难点。由于这些细胞抵御死亡，因此也就无法用化疗或放疗方法引发DNA损伤来杀死这些细胞。
席尔德-保尔特表示，虽然还需要进行更多的研究来充分了解这些蛋白的功能，但RanBPM能成为重新激活细胞凋亡、杀死癌细胞的靶标。此蛋白也可成为预测肿瘤是否会发展为恶性的一个标记。（生物谷Bioon.com）
生物谷推荐原始出处：
molecular cancer research December 2009; doi: 10.1158/1541-7786.MCR-09-0098
RanBPM Has Proapoptotic Activities That Regulate Cell Death Pathways in Response to DNA Damage
Elnaz Atabakhsh1,2, Dawn M. Bryce1, Karen J. Lefebvre2 and Caroline Schild-Poulter1,2
1Robarts Research Institute and 2Department of Biochemistry, The University of Western Ontario, London, Ontario, Canada
Ran-binding protein M (RanBPM) is a nucleocytoplasmic protein previously implicated in various signaling pathways, but whose function remains enigmatic. Here, we provide evidence that RanBPM functions as an activator of apoptotic pathways induced by DNA damage. First, transient expression of RanBPM in HeLa cells induced cell death through caspase activation, and in the long-term, forced expression of RanBPM impaired cell viability. RanBPM COOH-terminal domain stimulated the ability of RanBPM to induce caspase activation, whereas this activity was negatively regulated by the central SPRY domain. Second, small interfering RNA–directed knockdown of RanBPM prevented DNA damage–induced apoptosis, as evidenced by the marked reduction in caspase-3 and caspase-2 activation. This correlated with a magnitude fold increase in the survival of RanBPM-depleted cells. Following ionizing radiation treatment, we observed a progressive relocalization of RanBPM from the nucleus to the cytoplasm, suggesting that the activation of apoptotic pathways by RanBPM in response to ionizing radiation may be regulated by nucleocytoplasmic trafficking. Finally, RanBPM downregulation was associated with a marked decrease of mitochondria-associated Bax, whereas Bcl-2 overall levels were dramatically upregulated. Overall, our results reveal a novel proapoptotic function for RanBPM in DNA damage–induced apoptosis through the regulation of factors involved in the mitochondrial apoptotic pathway.
