E-cadherin engagement stimulates proliferation via Rac1.
E-cadherin engagement stimulates proliferation via Rac1.
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E-钙粘蛋白参与通过 Rac1 刺激增殖。
DOI：
10.1083/jcb.200510087
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发表时间：
2006-05-08
期刊：
影响因子：
--
通讯作者：
Chen CS
中科院分区：
文献类型：
--
作者：
Liu WF;Nelson CM;Pirone DM;Chen CS
E-钙粘蛋白与抑制肿瘤生长和抑制培养中的细胞增殖有关。我们观察到，逐渐降低正常大鼠肾-52E（NRK-52 E）或MCF-10A上皮细胞汇合的接种密度，确实可以释放生长停滞的细胞。出乎意料的是，接种密度的进一步降低使得细胞与相邻细胞分离降低了增殖。使用微工程基板的实验表明，E-钙粘蛋白的参与刺激在中间接种密度的增殖峰值，并在高密度的增殖停滞不涉及E-钙粘蛋白，而是导致从拥挤依赖性减少细胞扩散对底层基板。Rac 1的活性，这是诱导的E-钙粘蛋白的参与，特别是在中间接种密度，所需的钙粘蛋白刺激的增殖，和控制Rac 1激活E-钙粘蛋白介导的p120-连环蛋白。总之，这些研究结果证明了E-钙粘蛋白在增殖调节中的刺激作用，并确定了一种简单的机制，通过这种机制，细胞-细胞接触可以在不同的环境中触发或抑制上皮细胞增殖。
E-cadherin has been linked to the suppression of tumor growth and the inhibition of cell proliferation in culture. We observed that progressively decreasing the seeding density of normal rat kidney-52E (NRK-52E) or MCF-10A epithelial cells from confluence, indeed, released cells from growth arrest. Unexpectedly, a further decrease in seeding density so that cells were isolated from neighboring cells decreased proliferation. Experiments using microengineered substrates showed that E-cadherin engagement stimulated the peak in proliferation at intermediate seeding densities, and that the proliferation arrest at high densities did not involve E-cadherin, but rather resulted from a crowding-dependent decrease in cell spreading against the underlying substrate. Rac1 activity, which was induced by E-cadherin engagement specifically at intermediate seeding densities, was required for the cadherin-stimulated proliferation, and the control of Rac1 activation by E-cadherin was mediated by p120-catenin. Together, these findings demonstrate a stimulatory role for E-cadherin in proliferative regulation, and identify a simple mechanism by which cell–cell contact may trigger or inhibit epithelial cell proliferation in different settings.
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DOI：
10.1083/jcb.153.5.1049
发表时间：
2001-05-28
期刊：
The Journal of cell biology
影响因子：
--
作者：
Gottardi CJ;Wong E;Gumbiner BM
通讯作者：
Gumbiner BM
影响因子：
2.6
作者：
Boussadia, O;Kutsch, S;Kemler, R
通讯作者：
Kemler, R
影响因子：
11.4
作者：
Berx, G;CletonJansen, AM;vanRoy, F
通讯作者：
vanRoy, F
影响因子：
5.3
作者：
Bao, WJ;Thullberg, M;Strömblad, S
通讯作者：
Strömblad, S
DOI：
10.1083/jcb.200403043
发表时间：
2004-12-20
期刊：
The Journal of cell biology
影响因子：
--
作者：
Chu YS;Thomas WA;Eder O;Pincet F;Perez E;Thiery JP;Dufour S
通讯作者：
Dufour S