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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Microenvironmental modulation of asymmetric cell division in human lung cancer cells
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Microenvironmental modulation of asymmetric cell division in human lung cancer cells

机译：人肺癌细胞中不对称细胞分裂的微环境调节

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摘要

Normal tissue homeostasis is maintained through asymmetric cell divisions that produce daughter cells with differing self-renewal and differentiation potentials. Certain tumor cell subfractions can self-renew and repopulate the heterogeneous tumor bulk, suggestive of asymmetric cell division, but an equally plausible explanation is that daughter cells of a symmetric, division subsequently adopt differing cell fates. Cosegregation of template DNA during mitosis is one mechanism by which cellular components are segregated asymmetrically during cell division in fibroblast, muscle, mammary, intestinal, and neural cells. Asymmetric cell division of template DNA in tumor cells has remained elusive, however. Through pulse-chase experiments with halogenated thymidine analogs, we determined that a small population of cells within human lung cancer cell lines and primary tumor cell cultures asymmetrically divided their template DNA, which could be visualized in single cells and in real time. Template DNA cosegregation was enhanced by cell-cell contact. Its frequency was density-dependent and modulated by environmental changes, including serum deprivation and hypoxia. In addition, we found that isolated CD133~+ lung cancer cells were capable of tumor cell repopulation. Strikingly, during cell division, CD133 cosegregated with the template DNA, whereas the differentiation markers prosurfactant protein-C and pan-cytokeratins were passed to the opposing daughter cell, demonstrating that segregation of template DNA correlates with lung cancer cell fate. Our results demonstrate that human lung tumor cell fate decisions may be regulated during the cell division process. The characterization and modulation of asymmetric cell division in lung cancer can provide insight into tumor initiation, growth, and maintenance.
机译：正常组织的动态平衡是通过不对称细胞分裂来维持的，这种分裂会产生具有不同自我更新和分化潜能的子细胞。某些肿瘤细胞亚组分可以自我更新并重新填充异质肿瘤块，提示不对称细胞分裂，但同样合理的解释是，对称分裂的子细胞随后采用不同的细胞命运。模板DNA在有丝分裂期间的聚集是一种机制，通过该机制，成纤维细胞，肌肉，乳腺，肠和神经细胞的细胞分裂过程中细胞成分不对称地分离。但是，肿瘤细胞中模板DNA的不对称细胞分裂仍然难以捉摸。通过使用卤代胸腺嘧啶核苷类似物的脉冲追踪实验，我们确定了人类肺癌细胞系和原发性肿瘤细胞培养物中的一小部分细胞不对称地分裂了其模板DNA，可以在单个细胞中实时观察。模板DNA共分离通过细胞与细胞的接触得以增强。它的频率是密度依赖性的，并受环境变化的调节，包括血清缺乏和缺氧。此外，我们发现分离的CD133〜+肺癌细胞能够使肿瘤细胞重新聚集。令人惊讶的是，在细胞分裂过程中，CD133与模板DNA共分离，而分化标记物表面活性剂蛋白C和泛细胞角蛋白则传递给相对的子细胞，表明模板DNA的分离与肺癌细胞的命运有关。我们的结果表明，人肺肿瘤细胞的命运决定可能在细胞分裂过程中受到调节。肺癌中不对称细胞分裂的表征和调节可提供有关肿瘤起始，生长和维持的见解。

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  • 作者

    Sharon R. Pine; Brid M. Ryan; Lyuba Varticovski; Ana I. Robles; Curtis C. Harris;

  • 作者单位

    Laboratory of Human Carcinogenesis, Center for Cancer Research;

    rnLaboratory of Human Carcinogenesis, Center for Cancer Research Cancer Prevention Fellowship Program, Office of the Director, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892;

    rnLaboratory of Human Carcinogenesis, Center for Cancer Research Laboratory of Receptor Biology and Gene Expression, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892;

    rnLaboratory of Human Carcinogenesis, Center for Cancer Research;

    rnLaboratory of Human Carcinogenesis, Center for Cancer Research;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    cancer stem cell; CD133; immortal DNA; template DNA;

    机译：肿瘤干细胞;CD133;不朽的DNA模板DNA;

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