Annexin A1 attenuates EMT and metastatic potential in breast cancer.
作者： Sabine Maschler , Christoph A. Gebeshuber , Eva‐Maria Wiedemann , Memetcan Alacakaptan , Martin Schreiber
关键词: Intracellular vesicle 、 Gene knockdown 、 Metastasis suppressor 、 STAT3 、 Epithelial polarity 、 Biology 、 Annexin A1 、 Epithelial–mesenchymal transition 、 Cancer research 、 Metastasis
摘要: Metastasis is the major cause of carcinoma-induced death, but mechanisms involved are poorly understood. crucially involves epithelial-to-mesenchymal transition (EMT), causing loss epithelial polarity. Here we identify Annexin A1 (AnxA1), a protein with important functions in intracellular vesicle trafficking, as an efficient suppressor EMT and metastasis breast cancer. AnxA1 levels were strongly reduced mammary cells, metastatic murine human cell lines mouse carcinomas. RNAi-mediated knockdown cooperated oncogenic Ras to induce TGFβ-independent non-metastatic cells. Strikingly, forced expression carcinoma cells reversed abolished metastasis. stimulated multiple signalling pathways only Tyk2/Stat3 Erk1/2 essential for EMT.
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