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Elevated collagen-I augments tumor progressive signals intravasation and metastasis of prolactin-induced estrogen receptor alpha positive mammary tumor cells

机译:胶原蛋白I升高会增强催乳素诱导的雌激素受体α阳性乳腺肿瘤细胞的肿瘤进展信号血管内侵袭和转移

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摘要

BackgroundThe development and progression of estrogen receptor alpha positive (ERα+) breast cancer has been linked epidemiologically to prolactin. However, activation of the canonical mediator of prolactin, STAT5, is associated with more differentiated cancers and better prognoses. We have reported that density/stiffness of the extracellular matrix potently modulates the repertoire of prolactin signals in human ERα + breast cancer cells in vitro: stiff matrices shift the balance from the Janus kinase (JAK)2/STAT5 cascade toward pro-tumor progressive extracellular regulated kinase (ERK)1/2 signals, driving invasion. However, the consequences for behavior of ERα + cancers in vivo are not known.
机译:背景雌激素受体α阳性(ERα+)乳腺癌的发展和进展已在流行病学上与催乳素相关联。然而,催乳激素的经典调节因子STAT5的激活与分化程度更高的癌症和更好的预后相关。我们已经报道,细胞外基质的密度/刚度在体外有效地调节人ERα++乳腺癌细胞中催乳素信号的组成:刚性基质将平衡从Janus激酶(JAK)2 / STAT5级联转移到肿瘤进展的细胞外调节激酶(ERK)1/2信号,推动侵袭。但是,ERα++癌在体内的行为后果尚不明确。

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