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首页> 外文期刊>Journal of Cellular Physiology >Characterization of a novel amphiregulin-related molecule in 12-O-tetradecanoylphorbol-13-acetate-treated breast cancer cells.
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Characterization of a novel amphiregulin-related molecule in 12-O-tetradecanoylphorbol-13-acetate-treated breast cancer cells.

机译：amphiregulin-related特征的小说分子在12-O-tetradecanoylphorbol-13-acetate-treated乳腺癌细胞。

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摘要

Amphiregulin (AR) can be induced at the mRNA level by 17-beta-estradiol (E2) or the phorbol ester tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA). This study compares the effects of TPA and E2 on the regulation of processing of AR isoforms and on subcellular localization in human MCF-7 breast cancer cells. AR was localized in the nucleus of MCF-7 cells after E2 treatment, whereas it was predominantly secreted after TPA treatment. AR isoforms of 28, 18, and 10 kDa and an additional species of approximately 55-60 kDa were detected in the cellular conditioned media after TPA stimulation. Expression of this unusual AR isoform was inhibited by protein kinase C (PKC) inhibitors such as bryostatin or H-7. The biochemical properties of this isoform are consistent with it being an N-linked glycosylated form of the AR precursor that contains unprocessed mannose residues. The size of this large isoform is reduced to approximately 40 kDa after treating the TPA-induced MCF-7 cells with tunicamycin or treating the conditioned media of such cells with N-glycosidase F or with endoglycosidase H. Moreover, this isoform is able to blind several lectins with specificity for mannose residues. The 55-60 kDa glycosylated AR isoform, like lower Mr AR isoforms, is able to bind to heparin and to stimulate the growth of MCF-10A cells by interacting with the EGF receptor. These data suggest that TPA activation of PKC may be involved in post-translational modifications of AR, such as glycosylation, and in alteration of its subcellular routing to predominantly a secretory pathway.
机译：Amphiregulin (AR)可以诱导在mRNA水平17-beta-estradiol (E2)或佛波醇酯肿瘤促进剂12-O-tetradecanoylphorbol-13-acetate (TPA)。研究比较了TPA和E2的影响规定处理的基于“增大化现实”技术的亚型亚细胞定位在人类MCF-7乳房癌细胞。MCF-7 E2治疗后细胞,而主要分泌TPA治疗后。28日,18日亚型和10 kDa和一个额外的种约则高达55 - kDa被检测到TPA后细胞的媒体刺激。同种型抑制了蛋白激酶C (PKC)抑制剂如苔藓虫素或第7。生化特性的同种型符合它作为N-linked糖化形式的基于“增大化现实”技术的先驱,它包含未加工的甘露糖残基。大同种型是减少到大约40 kDa治疗后TPA-induced MCF-7细胞衣霉素或治疗条件的媒体这些细胞与N-glycosidase F或endoglycosidase h .此外,同种型能力盲数与特异性凝集素甘露糖残基。同种型降低AR亚型先生一样,是可以的结合肝素和刺激增长通过与EGF交互MCF-10A细胞受体。PKC可能参与翻译后修改的基于“增大化现实”技术,糖基化等变更的亚细胞的路由主要分泌途径。

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