作者: Haitao Zhang , Guo-Lei Zhou
DOI: 10.1038/SREP25933
关键词: Phosphorylation 、 Cell growth 、 MAPK/ERK pathway 、 Disease 、 Biology 、 Cell Cycle Protein 、 Cancer cell 、 Breast cancer 、 Cell biology 、 Cell
摘要: The actin-regulating protein CAP1 is implicated in the invasiveness of human cancers. However, exact role remains elusive and controversial given lines conflicting evidence. Moreover, a potential proliferative transformation has largely been overlooked. Further establishing dissecting underlying mechanisms are imperative before targeting can become possibility for cancer treatment. Here we report our findings that exerts cell type-dependent functions breast cells. Depletion metastatic MDA-MB-231 BT-549 cells stimulated while it actually inhibited non-metastatic MCF-7 or normal demonstrate proliferation anchorage-independent growth, again context-dependent manner. Importantly, identify pivotal roles ERK-centered signaling mediating both functions. Phosphor mutants at S307/S309 regulatory site had compromised rescue effects CAP1-knockdown cells, suggesting likely mediates upstream signals to control These novel mechanistic insights may ultimately open up avenues strategies treatment cancer, tailored specific types highly diverse disease.