Snail promotes cell migration through PI3K/AKT-dependent Rac1 activation as well as PI3K/AKT-independent pathways during prostate cancer progression.

作者: Veronica Henderson , Basil Smith , Liza J Burton , Diandra Randle , Marisha Morris

DOI: 10.1080/19336918.2015.1013383

关键词:

摘要: Snail, a zinc-finger transcription factor, induces epithelial-mesenchymal transition (EMT), which is associated with increased cell migration and metastasis in cancer cells. Rac1 small G-protein upon activation results formation of lamellipodia, the first protrusions formed by migrating We have previously shown that Snail promotes through down-regulation maspin tumor suppressor. hypothesized Snail's regulation may also involve signaling regulated PI3K/AKT and/or MAPK pathways. found overexpression LNCaP 22Rv1 prostate cells activity migration, inhibitor, NSC23766, could inhibit Snail-mediated migration. Conversely, downregulation using shRNA aggressive C4-2 decreased Moreover, ERK Treatment Snail-overexpressing LY294002, inhibitor or U0126, MEK significantly, but only LY294002 significantly reduced activity, suggesting via pathway. Furthermore, overexpressing displayed levels, while inhibition expression siRNA, led to PI3K/AKT, without affecting upstream PI3K/AKT. Overall, we dissected pathways promote alternatively PI3K/AKT-Rac1 involves This contribute progression.

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