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首页> 外文期刊>Journal of cellular biochemistry. >Caveolin-1 Mediates Inflammatory Breast Cancer Cell Invasion via the Akt1 Pathway and RhoC GTPase
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Caveolin-1 Mediates Inflammatory Breast Cancer Cell Invasion via the Akt1 Pathway and RhoC GTPase

机译：Caveolin-1通过Akt1途径和RhoC GTPase介导炎性乳腺癌细胞侵袭。

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With a propensity to invade the dermal lymphatic vessels of the skin overlying the breast and readily metastasize, inflammatory breast cancer (IBC) is arguably the deadliest form of breast cancer. We previously reported that caveolin-1 is overexpressed in IBC and that RhoC GTPase is a metastatic switch responsible for the invasive phenotype. RhoC-driven invasion requires phosphorylation by Akt1. Using a reliable IBC cell line we set out to determine if caveolin-1 expression affects RhoC-mediated IBC invasion. Caveolin-1 was down regulated by introduction of siRNA or a caveolin scaffolding domain. The ability of the cells to invade was tested and the status of Akt1 and RhoC GTPase examined. IBC cell invasion is significantly decreased when caveolin-1 is down regulated. Activation of Akt1 is decreased when caveolin-1 is down regulated, leading to decreased phosphorylation of RhoC GTPase. Thus, we report here that caveolin-1 overexpression mediates IBC cell invasion through activation Akt1, which phosphorylates RhoC GTPase. (C) 2015 Wiley Periodicals, Inc.
机译：炎性乳腺癌（IBC）具有侵入覆盖乳房的皮肤的真皮淋巴管并易于转移的倾向，可以说是最致命的乳腺癌形式。我们以前报道过，caveolin-1在IBC中过表达，RhoC GTPase是负责侵袭表型的转移开关。 RhoC驱动的入侵需要Akt1磷酸化。我们开始使用可靠的IBC细胞系来确定Caveolin-1表达是否影响RhoC介导的IBC侵袭。通过引入siRNA或Caveolin支架结构域，可降低Caveolin-1的表达。测试细胞入侵的能力，并检查Akt1和RhoC GTPase的状态。下调caveolin-1时，IBC细胞侵袭显着降低。当Caveolin-1下调时，Akt1的激活会降低，从而导致RhoC GTPase的磷酸化降低。因此，我们在这里报告小窝蛋白1过表达介导通过激活Akt1磷酸化RhoC GTPase的IBC细胞入侵。 （C）2015威利期刊公司

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