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CAPER, a novel regulator of human breast cancer progression

机译：CAPER，一种人类乳腺癌进展的新型调节剂

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CAPER is an estrogen receptor (ER) co-activator that was recently shown to be involved in human breast cancer pathogenesis. Indeed, we reported increased expression of CAPER in human breast cancer specimens. We demonstrated that CAPER was undetectable or expressed at relatively low levels in normal breast tissue and assumed a cytoplasmic distribution. In contrast, CAPER was expressed at higher levels in ductal carcinoma in situ (DCIS) and invasive ductal carcinoma (IDC) specimens, where it assumed a predominantly nuclear distribution. However, the functional role of CAPER in human breast cancer initiation and progression remained unknown. Here, we used a lentiviral-mediated gene silencing approach to reduce the expression of CAPER in the ER-positive human breast cancer cell line MCF-7. The proliferation and tumorigenicity of MCF-7 cells stably expressing control or human CAPER shRNAs was then determined via both in vitro and in vivo experiments. Knockdown of CAPER expression significantly reduced the proliferation of MCF-7 cells in vitro. Importantly, nude mice injected with MCF-7 cells harboring CAPER shRNAs developed smaller tumors than mice injected with MCF-7 cells harboring control shRNAs. Mechanistically, tumors derived from mice injected with MCF-7 cells harboring CAPER shRNAs displayed reduced expression of the cell cycle regulators PCNA, MCM7, and cyclin D1, and the protein synthesis marker 4EBP1. In conclusion, knockdown of CAPER expression markedly reduced human breast cancer cell proliferation in both in vitro and in vivo settings. Mechanistically, knockdown of CAPER abrogated the activity of proliferative and protein synthesis pathways.
机译：CAPER是一种雌激素受体（ER）共激活剂，最近被证明与人类乳腺癌的发病机理有关。确实，我们报道了CAPER在人类乳腺癌标本中的表达增加。我们证明，CAPER在正常乳腺组织中无法检测到或以相对较低的水平表达，并呈胞质分布。相比之下，CAPER在导管原位癌（DCIS）和浸润性导管癌（IDC）标本中的表达水平较高，假定其主要分布在核内。但是，CAPER在人类乳腺癌的发生和发展中的功能作用仍然未知。在这里，我们使用了慢病毒介导的基因沉默方法来减少ER阳性人类乳腺癌细胞MCF-7中CAPER的表达。然后通过体外和体内实验确定稳定表达对照或人CAPER shRNA的MCF-7细胞的增殖和致瘤性。敲低CAPER表达可显着降低体外MCF-7细胞的增殖。重要的是，注射了带有CAPER shRNA的MCF-7细胞的裸鼠比注射了带有控制shRNA的MCF-7细胞的鼠具有更小的肿瘤。从机理上讲，源自注射有CAPER shRNA的MCF-7细胞的小鼠的肿瘤显示出细胞周期调节剂PCNA，MCM7和cyclin D1以及蛋白合成标记4EBP1的表达降低。总之，在体外和体内环境中，敲低CAPER表达均可显着降低人乳腺癌细胞的增殖。从机制上讲，敲低CAPER废除了增殖和蛋白质合成途径的活动。

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