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External and internal EGFR-activating signals drive mammary epithelial cells proliferation and viability
Molecular and Cellular Endocrinology ( IF 4.1 ) Pub Date : 2020-11-09 , DOI: 10.1016/j.mce.2020.111081
Alessia Morato 1 , Eugenio Martignani 1 , Silvia Miretti 1 , Mario Baratta 1 , Paolo Accornero 1
Affiliation  

During puberty, the mammary gland undergoes an intense growth, dependent on the interplay between the Epidermal Growth Factor Receptor (EGFR) in the stroma and different mammary epithelial receptors. We hypothesize that EGFR expressed in the mammary epithelium also has a role in puberty and the epithelial cells can self-sustain by EGFR-mediated autocrine signaling. We adopted mammary cell lines from different species, as in vitro model for the epithelium, and we observed that EGFR-signaling positively affects their survival and proliferation. Once deprived of external growth factors, mammary cells still showed strong Erk 1/2 phosphorylation, abolished upon EGFR inhibition, coupled with a further reduction in survival and proliferation. Based on gene expression analysis, three EGFR-ligands (AREG, EREG and HBEGF) are likely to mediate this autocrine signaling. In conclusion, internal EGFR-activating signals sustain mammary epithelial cell proliferation and survival in vitro.



中文翻译:

外部和内部 EGFR 激活信号驱动乳腺上皮细胞增殖和活力

在青春期,乳腺会经历强烈的生长,这取决于基质中的表皮生长因子受体 (EGFR) 和不同的乳腺上皮受体之间的相互作用。我们假设在乳腺上皮中表达的 EGFR 在青春期也有作用,并且上皮细胞可以通过 EGFR 介导的自分泌信号自我维持。我们采用了来自不同物种的乳腺细胞系,如体外上皮模型,我们观察到 EGFR 信号对它们的存活和增殖产生积极影响。一旦剥夺了外部生长因子,乳腺细胞仍然表现出强烈的 Erk 1/2 磷酸化,在 EGFR 抑制后消失,同时存活和增殖进一步降低。根据基因表达分析,三种 EGFR 配体(AREG、EREG 和 HBEGF)可能介导这种自分泌信号传导。总之,内部 EGFR 激活信号在体外维持乳腺上皮细胞增殖和存活。

更新日期:2020-11-09
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