Cellular anchorage sensing and anoikis
Cellular anchorage sensing and anoikis
复制标题
细胞锚定传感和失巢凋亡
DOI：
10.1007/s11805-011-0552-1
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发表时间：
2011
期刊：
影响因子：
--
通讯作者：
Zhenyi Ma
中科院分区：
文献类型：
--
作者：
W. Du;Zhichao Zheng;Zhe Liu;Zhenyi Ma
失去与细胞外基质的整合素依赖性锚定的正常上皮细胞会引发失巢凋亡，而转移性肿瘤细胞则绕过失巢凋亡途径，这是实现转移的关键事件之一。失巢凋亡的生理作用也涉及胚胎发育和组织稳态，这表明失巢凋亡必须在某种程度上受到严格调控。尽管其重要性，但人们对失巢调控和报告锚定丧失的近端信号所涉及的分子途径知之甚少。最近的研究表明，位于粘着斑的接头蛋白 p66Shc 通过激活 RhoA 介导失巢凋亡。然而，p66Shc在转移性癌细胞中表达不足，无法启动失巢凋亡并促进肿瘤转移。促凋亡蛋白p66Shc的重新表达可以恢复失巢凋亡的易感性。因此，p66Shc可能是诊断肿瘤转移和肿瘤治疗的潜在靶分子。
Normal epithelial cells that lose the integrindependent anchorage to their extracellular matrix trigger anoikis, while metastatic tumor cells bypass anoikis pathway, which is one of the key events to achieve the metastasis. Physiological role of anoikis is also involved during embryonic development and tissue homeostasis, suggesting that anoikis must be strictly regulated at some level. Despite its importance, the molecular pathways involved in the regulation of anoikis and the proximal signals reporting loss of anchorage are poorly understood. Recent studies suggest an adaptor protein p66Shc, localizing at focal adhesions, mediates anoikis through activation of RhoA. However, expression of p66Shc is inadequate in metastatic cancer cells, failing to initiate anoikis and promoting tumor metastasis. Reexpression of proapoptotic protein p66Shc can restore the susceptibility to anoikis. Thus, p66Shc may be a potential target molecule for diagnosis of tumor metastasis and for tumor treatment.
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影响因子：
3.7
作者：
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通讯作者：
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DOI：
--
发表时间：
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期刊：
Clinical cancer research : an official journal of the American Association for Cancer Research
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作者：
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通讯作者：
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DOI：
--
发表时间：
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期刊：
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影响因子：
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通讯作者：
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影响因子：
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作者：
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