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首頁(yè)> 美國(guó)衛(wèi)生研究院文獻(xiàn)>Molecular and Cellular Biology >Activation of β-Catenin Signaling in Prostate Cancer by Peptidyl-Prolyl Isomerase Pin1-Mediated Abrogation of the Androgen Receptor-β-Catenin Interaction
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Activation of β-Catenin Signaling in Prostate Cancer by Peptidyl-Prolyl Isomerase Pin1-Mediated Abrogation of the Androgen Receptor-β-Catenin Interaction

機(jī)譯：肽基脯氨酰異構(gòu)酶Pin1介導(dǎo)的雄激素受體-β-Catenin相互作用的抑制作用激活前列腺癌中的β-Catenin信號(hào)傳導(dǎo)。

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Androgen receptor (AR) interacts with β-catenin and can suppress its coactivation of T cell factor 4 (Tcf4) in prostate cancer (PCa) cells. Pin1 is a peptidyl-prolyl cis/trans isomerase that stabilizes β-catenin by inhibiting its binding to the adenomatous polyposis coli gene product and subsequent glycogen synthase kinase 3β (GSK-3β)-dependent degradation. Higher Pin1 expression in primary PCa is correlated with disease recurrence, and this study found that Pin1 expression was markedly increased in metastatic PCa. Consistent with this result, increased expression of Pin1 in transfected LNCaP PCa cells strongly accelerated tumor growth in vivo in immunodeficient mice. Pin1 expression in LNCaP cells enhanced β-catenin/Tcf4 transcriptional activity, as assessed using Tcf4-regulated reporter genes, and increased expression of endogenous Tcf4 and c-myc. However, in contrast to results in cells with intact PTEN and active GSK-3β, Pin1 expression in LNCaP PCa cells, which are PTEN deficient, did not increase β-catenin. Instead, Pin1 expression markedly inhibited the β-catenin interaction with AR, and Pin1 abrogated the ability of AR to antagonize β-catenin/Tcf4 binding and transcriptional activity. These findings demonstrate that AR can suppress β-catenin signaling, that the AR-β-catenin interaction can be regulated by Pin1, and that abrogation of this interaction can enhance β-catenin/Tcf4 signaling and contribute to aggressive biological behavior in PCa.
機(jī)譯：雄激素受體（AR）與β-catenin相互作用，可以抑制前列腺癌（PCa）細(xì)胞中T細(xì)胞因子4（Tcf4）的共激活。 Pin1是一種肽基-脯氨酰順/反異構(gòu)酶，可通過(guò)抑制其與腺瘤性息肉病大腸桿菌基因產(chǎn)物的結(jié)合以及隨后的糖原合酶激酶3β（GSK-3β）依賴性降解來(lái)穩(wěn)定β-catenin。原發(fā)性PCa中較高的Pin1表達(dá)與疾病復(fù)發(fā)相關(guān)，這項(xiàng)研究發(fā)現(xiàn)，轉(zhuǎn)移性PCa中Pin1表達(dá)顯著增加。與此結(jié)果一致，在免疫缺陷小鼠體內(nèi)，轉(zhuǎn)染的LNCaP PCa細(xì)胞中Pin1表達(dá)的增加強(qiáng)烈促進(jìn)了體內(nèi)腫瘤的生長(zhǎng)。使用Tcf4調(diào)節(jié)的報(bào)告基因評(píng)估，LNCaP細(xì)胞中Pin1的表達(dá)增強(qiáng)了β-catenin/ Tcf4的轉(zhuǎn)錄活性，并增加了內(nèi)源性Tcf4和c-myc的表達(dá)。但是，與具有完整PTEN和活性GSK-3β的細(xì)胞的結(jié)果相反，PTEN缺陷的LNCaP PCa細(xì)胞中的Pin1表達(dá)并未增加β-catenin。相反，Pin1表達(dá)明顯抑制了β-catenin與AR的相互作用，Pin1消除了AR拮抗β-catenin/ Tcf4結(jié)合和轉(zhuǎn)錄活性的能力。這些發(fā)現(xiàn)表明AR可以抑制β-catenin信號(hào)傳導(dǎo)，AR-β-catenin相互作用可以由Pin1調(diào)節(jié)，并且這種相互作用的消除可以增強(qiáng)β-catenin/ Tcf4信號(hào)傳導(dǎo)并有助于PCa的侵襲性生物學(xué)行為。

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