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Aurora B-Induced Cytokinesis Defects in Malignant Cells

Aurora B 诱导的恶性肿瘤细胞胞质分裂缺陷

基本信息

批准号：
8425107
负责人：
WILLIAM SAUNDERS
金额：
$ 35.01万
依托单位：
UNIVERSITY OF PITTSBURGH AT PITTSBURGH
依托单位国家：
美国
项目类别：
财政年份：
2004
资助国家：
美国
起止时间：
2004-07-01 至 2016-02-29
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8425107
关键词：
American Area Back Beryllium Bypass Cancer Biology Cancer cell line Categories Cell Proliferation Cell division Cells Centrosome Chromatin Chromosomal Instability Cytokinesis DNA Damage Data Defect Dependence Disease Drops Electrophoresis Event Evolution Excision Failure Filament Genetic Genomic Instability Goals Human Cell Line Immunofluorescence Immunologic In Vitro Investigation Lead Link Malignant Neoplasms Measures Mitotic Molecular Motor Mus Myosin ATPase Myosin Light Chain Kinase Myosin Light Chains Myosin Regulatory Light Chains Non-Malignant Normal Cell One-Step dentin bonding system Pathway interactions Phosphorylation Phosphotransferases Polyploidy Procedures Protein Dephosphorylation Publishing Role Small Interfering RNA Source Staining method Stains Testing Time Work c-myc Genes cancer cell cell type design inhibitor/antagonist inner centromere protein inorganic phosphate killings meetings myosin phosphatase neoplastic cell overexpression prevent prognostic public health relevance therapy resistant tumor tumorigenesis

项目摘要

DESCRIPTION (provided by applicant): This application is a renewal of an ongoing project to understand mitotic or cell division defects in cancer. Our goals are to identify the source of the defects and their impact on oncogenesis. Within this broad category, the project will focus on the source of centrosome amplification and polyploidy. This is a newly emerging area of cancer biology and the mechanisms are poorly understood. Both cancer and normal cells grown in culture will be investigated. We have shown that cancer cells often fail to divide properly because of defects in regulatory myosin light chain phosphorylation. We believe that this is due to inhibition of the kinase responsible for adding the phosphate to the myosin light chain. We propose to determine how this kinase is inhibited in tumor cells. If the mistakes in division are understood, we might be able to prevent the abnormal proliferation of cells in tumors.

描述（由申请人提供）：本申请是一个正在进行的项目，以了解癌症有丝分裂或细胞分裂缺陷的更新。我们的目标是确定缺陷的来源及其对肿瘤发生的影响。在这个广泛的类别中，该项目将集中在中心体扩增和多倍性的来源。这是一个新兴的癌症生物学领域，其机制知之甚少。将研究在培养物中生长的癌细胞和正常细胞。我们已经发现，由于调节肌球蛋白轻链磷酸化的缺陷，癌细胞通常不能正常分裂。我们认为这是由于抑制了负责将磷酸加入肌球蛋白轻链的激酶。我们建议确定这种激酶在肿瘤细胞中是如何被抑制的。如果我们了解了分裂中的错误，我们就有可能防止肿瘤细胞的异常增殖。