Zhao Xiansi, Ayer Robert E, Davis Shannon L, Ames Sarah J, Florence Brian, Torchinsky Cyrus, Liou James S, Shen Ling, Spanjaard Remco A
Department of Otolaryngology and Biochemistry, Cancer Research Center, Boston University School of Medicine, Boston, MA 02118, USA.
Cancer Res. 2005 Mar 15;65(6):2125-9. doi: 10.1158/0008-5472.CAN-04-3377.
p53 is a critical tumor suppressor which removes cells with DNA damage by regulating expression and activity of a select group of p53-induced genes (PIG) that subsequently induce apoptosis. PIG8 was also identified as a gene induced by etoposide and named etoposide-induced gene 24 (EI24). Later experiments established EI24/PIG8 as a proapoptotic factor and suggested that it may function as a tumor suppressor. Indeed, EI24/PIG8 is relatively highly mutated in aggressive breast cancers and is located in a region which expresses frequent loss of heterozygosity. However, despite these important observations, the activity and role of EI24/PIG8 remain largely unknown. We used (immmuno)fluorescence microscopy and subcellular fractionation techniques to show that EI24/PIG8 is localized in the endoplasmic reticulum (ER). Pull-down experiments showed that it specifically binds with Bcl-2, a death regulator known to reside in mitochondria, ER, and the nuclear envelope. EI24/PIG8-Bcl-2 binding was corroborated by coimmunoprecipitation and other in vitro and in vivo protein-protein binding assays. Further analysis showed that EI24/PIG8 uses its N-terminal region to bind the BH3 domain in Bcl-2. Finally, we used immunohistochemical techniques to analyze expression of EI24/PIG8 in breast cancer tissue progression arrays and showed that loss of EI24/PIG8 is associated with tumor invasiveness but not with the development of the primary tumor. These results suggest that EI24/PIG8 is a novel, ER-localized Bcl-2-binding protein which may contribute to apoptosis by modulating the activity and/or function of Bcl-2 in this organelle. EI24/PIG8 may serve to prevent tumor spreading, consistent with its suspected role as a tumor suppressor.
p53是一种关键的肿瘤抑制因子,它通过调节一组特定的p53诱导基因(PIG)的表达和活性来清除DNA受损的细胞,这些基因随后诱导细胞凋亡。PIG8也被鉴定为依托泊苷诱导的基因,并被命名为依托泊苷诱导基因24(EI24)。后来的实验确定EI24/PIG8为促凋亡因子,并表明它可能作为肿瘤抑制因子发挥作用。事实上,EI24/PIG8在侵袭性乳腺癌中相对高度突变,且位于一个经常发生杂合性缺失的区域。然而,尽管有这些重要发现,EI24/PIG8的活性和作用在很大程度上仍不清楚。我们使用(免疫)荧光显微镜和亚细胞分级分离技术表明EI24/PIG8定位于内质网(ER)。下拉实验表明它与Bcl-2特异性结合,Bcl-2是一种已知存在于线粒体、内质网和核膜中的死亡调节因子。EI24/PIG8与Bcl-2的结合通过共免疫沉淀以及其他体外和体内蛋白质-蛋白质结合试验得到证实。进一步分析表明EI24/PIG8利用其N端区域与Bcl-2中的BH3结构域结合。最后,我们使用免疫组织化学技术分析EI24/PIG8在乳腺癌组织进展阵列中的表达,结果表明EI24/PIG8的缺失与肿瘤侵袭性相关,但与原发性肿瘤的发生无关。这些结果表明EI24/PIG8是一种新型的、内质网定位的Bcl-2结合蛋白,它可能通过调节该细胞器中Bcl-2的活性和/或功能来促进细胞凋亡。EI24/PIG8可能有助于防止肿瘤扩散,这与其作为肿瘤抑制因子的推测作用一致。