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首页> 外文期刊>Journal of Cellular Physiology >Radiation-Induced RhoGDI beta Cleavage Leads to Perturbation of Cell Polarity: A Possible Link to Cancer Spreading
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Radiation-Induced RhoGDI beta Cleavage Leads to Perturbation of Cell Polarity: A Possible Link to Cancer Spreading

机译：辐射诱导RhoGDIβ乳沟导致细胞极性的扰动:一个可能的链接癌症扩散

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The equilibrium between proliferation and apoptosis is tightly balanced to maintain tissue homeostasis in normal tissues and even in tumors. Achieving and maintaining such a balance is important for cancer regrowth and spreading after cytotoxic treatments. Caspase-3 activation and tumor cell death following anticancer therapy as well as accompanying cell death pathways are well characterized, but their association to homeostasis of cancerous tissue and tumor progression remains poorly understood. Here we proposed a novel mechanism of cancer spreading induced by caspase-3. RhoGDI beta, known as a direct cleavage substrate of caspase-3, is overexpressed in many epithelial cancers. The N-terminal-truncated RhoGDI beta (Delta N-RhoGDI beta) is accumulated in caspase-3-activated cells. Stable expression of Delta N-RhoGDI beta in HeLa cells did not induce apoptosis, but impaired directional cell migration in a wound-healing assay accompanied by a perturbed direction of cell division at the wound edge. Subcellular protein fractionation experiments revealed that Delta N-RhoGDI beta but not wild-type RhoGDI beta was present in the detergent-soluble cytoplasmic and nuclear fractions and preferentially associated with Cdc42. Furthermore, Cdc42 activity was constitutively inhibited by stable expression of Delta N-RhoGDI beta, resulting in increased radiation-induced compensatory proliferation linking to RhoA activation. Thus, Delta N-RhoGDI beta dominant-negatively regulates Cdc42 activity and contributes to loss of polarity-related functions. The caspase-3-cleaved RhoGDI beta is a possible determinant to promote cancer spreading due to deregulation of directional organization of tumor cell population and inhibition of default equilibrium between proliferation and apoptosis after cytotoxic damage. (C) 2016 Wiley Periodicals, Inc.
机译：核扩散和之间的平衡细胞凋亡是紧平衡的维护组织体内平衡在正常组织,甚至肿瘤。实现和维护这种平衡重要的癌症后再生和传播细胞毒性治疗。抗癌治疗后肿瘤细胞死亡以及伴随细胞死亡通路特征,但他们的协会癌组织和肿瘤的体内平衡发展仍然知之甚少。提出了一种新颖的癌症扩散机制caspase-3引起的。直接劈理caspase-3衬底,在许多上皮癌。N-terminal-truncated RhoGDIβ(δN-RhoGDIβ)是caspase-3-activated积累细胞。在海拉细胞不诱导细胞凋亡,但是受损细胞定向迁移的愈合分析伴随着摄动在伤口边缘细胞分裂方向。亚细胞蛋白质分离实验透露,三角洲N-RhoGDIβ但不是野生型RhoGDIβ是存在的detergent-soluble细胞质和核分数和优先Cdc42。持续被稳定的表达δN-RhoGDIβ,导致增加辐射诱导补偿扩散链接到RhoA激活。βdominant-negatively调节Cdc42活动并有助于polarity-related的损失功能。可能的因素促进癌症扩散由于定向组织的管制的人口和抑制肿瘤细胞默认的扩散和平衡细胞毒性损伤后细胞凋亡。期刊、公司。

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