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首页> 外文学位 >Polarity and proliferation are controlled by distinct signaling pathways downstream of PI3-kinase in breast epithelial tumor cells: Functional bifurcation of PI3-kinase signaling pathway.
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Polarity and proliferation are controlled by distinct signaling pathways downstream of PI3-kinase in breast epithelial tumor cells: Functional bifurcation of PI3-kinase signaling pathway.

机译：极性和增殖受乳腺上皮肿瘤细胞中PI3激酶下游不同信号通路的控制：PI3激酶信号通路的功能分叉。

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摘要

Epithelial tumorigenesis is a combination of multiple genetic lesions leading to aberrant proliferation, failure to differentiate, and loss of tissue architecture/polarity and tissue-specific function. Although it is well established that aberrant proliferation is one of the most prominent feature of most cancers and that dysregulated cell proliferation control machineries are the major driving force of tumorigenesis, it is not clear whether deregulated proliferation is sufficient to initiate all tumorigenic phenotypes, or whether polarity defect is an independent factor that also contributes to cancer development.; The proper development and maintenance of polarity is essential for the formation of tissue-specific structures, organization integrity, and tissue functiona. Polarity defects are a hallmark of epithelial cancers and not only lead to loss of tissue organization/polarity and function, but also cause spatial disorganization of signaling pathways that control cell proliferation and indirectly affect cellular proliferation so as to increase the potential of cells to proceed to aggressive tumors.; Overexpression or aberrant activation of many kinases have been found in a variety of human cancers including breast cancers, and has been shown to transform mammalian cells and cause tumor development in mice. The multiple functions of each oncogenic kinase predicts that the ultimate formation of a tumor may not be the result of simply deregulated proliferation, the most prominent feature controlled by oncogenic kinases, but also the result of convergence of all the phenotypic defects caused by downstream effectors with distinct functions. However, it is unclear whether deregulated proliferation is the sole cause of other tumor-causing defects, such as loss of tissue achitecture and polarity. My thesis aims to investigate whether altered proliferation is sufficient to change tissue polarity or whether deregulation of polarity is an independent, separable variable contributing to breast cancer development. (Abstract shortened by UMI.)
机译：上皮肿瘤发生是多种遗传损伤的组合，导致异常增殖，分化失败以及组织结构/极性和组织特异性功能的丧失。尽管已经公认异常增殖是大多数癌症的最显着特征之一，并且细胞增殖控制机制失调是肿瘤发生的主要驱动力，但尚不清楚失调的增殖是否足以启动所有致瘤表型，或者是否极性缺陷是一个独立的因素，也有助于癌症的发展。极性的正确发展和维持对于组织特异性结构的形成，组织完整性和组织功能至关重要。极性缺陷是上皮癌的标志，不仅导致组织组织/极性和功能的丧失，而且还导致控制细胞增殖并间接影响细胞增殖的信号传导途径的空间混乱，从而增加了细胞继续发展的潜力。侵袭性肿瘤。在包括乳腺癌在内的多种人类癌症中发现了许多激酶的过度表达或异常激活，并且已证明它们可以转化哺乳动物细胞并引起小鼠肿瘤的发展。每种致癌激酶的多种功能都预示着肿瘤的最终形成可能不是简单的增殖失控（致癌激酶控制的最突出特征）的结果，而是下游效应子引起的所有表型缺陷趋同的结果。独特的功能。然而，尚不清楚增殖失调是否是其他引起肿瘤的缺陷（例如组织结构和极性丧失）的唯一原因。我的论文旨在研究改变的增殖是否足以改变组织的极性，或者极性的失调是否是有助于乳腺癌发展的独立且可分离的变量。 （摘要由UMI缩短。）

著录项

  • 作者

    Liu, Hong.;

  • 作者单位

    University of California, Berkeley.;

  • 授予单位 University of California, Berkeley.;
  • 学科 Biology Cell.; Biology Molecular.
  • 学位 Ph.D.
  • 年度 2005
  • 页码 197 p.
  • 总页数 197
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞生物学;分子遗传学;
  • 关键词

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