Metastasis-Inducing Mts1/S100A4 Protein Binds to Tumor Suppressor p53 Protein
作者： M. Grigorian , E. Lukanidin
关键词: E2F1 、 CD30 、 SOCS5 、 Cancer research 、 Retinoblastoma-like protein 1 、 Reporter gene 、 SOCS6 、 Biology 、 Promyelocytic leukemia protein 、 Tumor progression
摘要: This study for the first time demonstrates a physical and functional interaction between Ca2+-binding protein Mts1/S100A4 tumor suppressor p53 protein. Using different in vitro vivo approaches, we have found that Mts1 can bind to C-terminal regulatory domain of p53. The binding promotes activation reporter gene transcription vivo. A modulation target (p21/WAF,bax,mdm-2, thrombospondin-1) expression was observed upon induction cells expressing wild-type These results suggest ability enhance p53-dependent apoptosis leads decrease/disappearance Thus, selection more aggressive, metastatic phenotype during progression.
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