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首页> 外文期刊>Journal of Cellular Physiology >Knock-down of amphiregulin inhibits cellular invasion in inflammatory breast cancer.
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Knock-down of amphiregulin inhibits cellular invasion in inflammatory breast cancer.

机译：amphiregulin抑制细胞的混战炎性乳腺癌的入侵。

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We have previously shown that SUM-149 human breast cancer cells require an amphiregulin (AREG) autocrine loop for cell proliferation. We also demonstrated that AREG can increase epidermal growth factor receptor (EGFR) stability and promote EGFR localization to the plasma membrane. In the present studies we successfully knocked-down AREG expression in SUM-149 cells by lentiviral infection of AREG shRNA. In the absence of AREG expression, SUM-149 cell growth was slowed, but not completely inhibited. Furthermore, cells infected with AREG shRNA constructs showed an increase in EGFR protein expression by Western blot. Immunofluorescence and confocal microscopy showed that following AREG knock-down, EGFR continued to localize to the cell surface. Soft agar assays demonstrated that AREG knock-down cells retain anchorage-independent growth capacity. Additionally mammosphere forming assays and Adefluor staining analysis showed that knock-down of AREG expression did not affect the expression of stem cell phenotypes. However, following AREG knock-down, SUM-149 cells demonstrated a dramatic decrease in their ability to invade a Matrigel matrix. Consistent with this observation, microarray analysis comparing cells infected with a non-silencing vector to the AREG knock-down cells, identified genes associated with the invasive phenotype such as RHOB and DKK1, and networks associated with cell motility such as integrin-linked kinase signaling, and focal adhesion kinase signaling. AREG was also found to modulate WNT and Notch signaling in these cells. Thus, AREG functions in regulating the invasive phenotype, and we propose that this regulation may be through altered signaling that occurs when AREG activates plasma membrane localized EGFR.
机译：我们以前显示总和- 149人类乳房肿瘤细胞需要一个amphiregulin(沙土荒漠)自分泌环细胞增殖。证明了沙土荒漠可以增加表皮生长因子受体(EGFR)和稳定促进表皮生长因子受体定位到质膜。在目前的研究中我们成功拆装的沙土荒漠表达式总之- 149细胞慢病毒感染的沙土荒漠成分。缺乏沙土荒漠的表情,和- 149细胞生长放缓,但没有完全抑制。此外,细胞感染沙土荒漠成分构造了EGFR蛋白的增加通过免疫印迹表达。和共焦显微镜显示沙土荒漠混战,EGFR继续本地化细胞表面。保留,沙土荒漠压倒一切的细胞anchorage-independent增长能力。此外mammosphere化验和形成Adefluor染色分析表明,可拆卸的沙土荒漠的表达并不影响表达式干细胞表型。演示了一个戏剧性的混战,总和- 149细胞减少他们入侵人工基底膜的能力矩阵。微阵列分析比较细胞感染non-silencing向量的沙土荒漠混战细胞,确定相关基因侵入性表型,如RHOB DKK1,网络等与细胞活性有关integrin-linked激酶信号和焦点黏附激酶信号。在这些细胞调节WNT和Notch信号。因此,沙土荒漠功能调节的入侵表型,我们建议本条例可能是通过改变信号发生在吗沙土荒漠激活等离子体膜局部表皮生长因子受体。

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