Cyr61 promotes growth of pancreatic carcinoma via nuclear exclusion of p27
作者： Weidong Shi , Jianhua Yin , Zhen Chen , Hao Chen , Luming Liu
DOI: 10.1007/S13277-014-2423-X
关键词: MAPK/ERK pathway 、 Cancer research 、 Cell biology 、 Signal transduction 、 Biology 、 Cell cycle 、 Kinase 、 Cell growth 、 Protein kinase B 、 PI3K/AKT/mTOR pathway 、 Protein kinase A
摘要: The molecular regulation of the growth pancreatic carcinoma (PCC) is complicated and not defined yet. Here we show that cysteine-rich protein 61 (Cyr61) levels were significantly higher in PCC than adjacent nontumor tissues from same human patient. Overexpression Cyr61 enhanced proliferation cells, while inhibition decreased cells. Further analysis showed seemed to activate phosphatidylinositol 3-kinase (PI3K) but extracellular-related kinase/mitogen-activated kinase (ERK/MAPK) signaling pathway which subsequently induced nuclear exclusion a major cell cycle inhibitor, p27, increase proliferation. Taken together, these findings reveal basis underlying Cyr61-regulated proliferation, suggest potential role growth, highlight as novel target for therapy.
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