miR-15和miR-16通过靶向BCL2诱导细胞凋亡。
miR-15 and miR-16 induce apoptosis by targeting BCL2.
作者信息
Cimmino Amelia, Calin George Adrian, Fabbri Muller, Iorio Marilena V, Ferracin Manuela, Shimizu Masayoshi, Wojcik Sylwia E, Aqeilan Rami I, Zupo Simona, Dono Mariella, Rassenti Laura, Alder Hansjuerg, Volinia Stefano, Liu Chang-Gong, Kipps Thomas J, Negrini Massimo, Croce Carlo M
机构信息
Department of Molecular Virology, Immunology, and Medical Genetics and Comprehensive Cancer Center, Ohio State University, Columbus OH 43210, USA.
出版信息
Proc Natl Acad Sci U S A. 2005 Sep 27;102(39):13944-9. doi: 10.1073/pnas.0506654102. Epub 2005 Sep 15.
Chronic lymphocytic leukemia (CLL) is the most common human leukemia and is characterized by predominantly nondividing malignant B cells overexpressing the antiapoptotic B cell lymphoma 2 (Bcl2) protein. miR-15a and miR-16-1 are deleted or down-regulated in the majority of CLLs. Here, we demonstrate that miR-15a and miR-16-1 expression is inversely correlated to Bcl2 expression in CLL and that both microRNAs negatively regulate Bcl2 at a posttranscriptional level. BCL2 repression by these microRNAs induces apoptopsis in a leukemic cell line model. Therefore, miR-15 and miR-16 are natural antisense Bcl2 interactors that could be used for therapy of Bcl2-overexpressing tumors.
慢性淋巴细胞白血病（CLL）是最常见的人类白血病，其特征是主要为不分裂的恶性B细胞，这些细胞过度表达抗凋亡的B细胞淋巴瘤2（Bcl2）蛋白。在大多数慢性淋巴细胞白血病中，miR-15a和miR-16-1缺失或下调。在此，我们证明miR-15a和miR-16-1的表达与慢性淋巴细胞白血病中Bcl2的表达呈负相关，并且这两种微小RNA在转录后水平上对Bcl2进行负调控。在白血病细胞系模型中，这些微小RNA对BCL2的抑制可诱导细胞凋亡。因此，miR-15和miR-16是天然的Bcl2反义相互作用分子，可用于治疗Bcl2过表达的肿瘤。
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