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</svg></a></li> </ul> </div> <div class="col-12 mt-2 mt-xl-3"> <hr> </div> <div class="col-12 mt-3 mb-5 mb-lg-0"> <article class="news-article"> <div class="article__info mb-2"> <div class="article__info-item mr-auto"> <a href="//www.puressens.com/archive/05-12-2022/" rel="nofollow"> <svg class="article__info-icon"> <use href="https://medx.b-cdn.net/tmpl/v6/img/svg/sprite.svg#icon_clock" x="0" y="0"></use> </svg></a> <p class="text-uppercase text-low">2022年12月5日</gydF4y2Bap> </div> </div> <h1 class="text-extra-large line-low mb-2">关于癌细胞如何以及为什么扩散发现了新的线索</h1gydF4y2Ba> <p class="article-byline text-low">吉莉安·卢瑟福，<一个cl一个ss="article-byline__link" href="http://www.ualberta.ca/" target="_blank">阿尔伯塔大学</一个></p> <div class="mt-4 article-main"> <div class="article-gallery lightGallery"> <div data-thumb="https://scx1.b-cdn.net/csz/news/tmb/2022/new-clue-discovered-fo.jpg" data-src="https://scx2.b-cdn.net/gfx/news/hires/2022/new-clue-discovered-fo.jpg" data-sub-html="Viscosity enhances cell migration and promotes an ARP2/3-mediated dense actin network at the leading edge. <b>a</b>,<b>b</b>, Speeds of MDA-MB-231 cells (<b>a</b>) and other indicated cell types (<b>b</b>) inside confining channels at prescribed viscosities. The red lines represent the median of ≥69 cells from ≥3 experiments. <b>c</b>, Cell trajectories on 2D collagen-coated surfaces after 10 h. <b>d</b>, Cells disseminating from 3D spheroids. <b>e</b>, The time required for the first cell dissociation from each spheroid (<i>n</i> ≥ 53) from 3 experiments. <b>f</b>, Airyscan images of phalloidin stained cells on collagen-coated substrates. The red arrow indicates high F-actin staining along the cell edge. <b>g</b>, The fraction of cell-projected area with a Lifeact–GFP-rich lamella for <i>n</i> ≥ 28 cells from 3 experiments. <b>h</b>, The leading edge of Lifeact–GFP-expressing cells on collagen-coated surfaces at <i>t</i> = 0 min (red) and <i>t</i> = 2 min (cyan) (left). Right, leading-edge lamella growth in <i>n</i> ≥ 19 cells from 3 experiments. Data are the moving average ± s.e.m. <i>P</i> < 0.05 for all points <i>t</i> ≥ 50 s. Time is shown as min:s. <b>i</b>,<b>j</b>, STORM reconstruction (<b>i</b>) and density quantification (<b>j</b>) of F-actin for cells (<i>n</i> ≥ 13) on substrates from 2 experiments. <b>k</b>, The average actin density over time from 20 stochastic simulations. Viscous forces were applied at <i>t</i> = 6 s (red arrow) and maintained until the end of the simulation. <b>l</b>, Confocal images of cells expressing Lifeact–GFP and ARP3–mCherry in confinement. The red arrow indicates high ARP3 intensity at leading-edge protrusions at 8 cP. <b>m</b>, The relative ARP3–mCherry intensity along normalized cell length in confined cells. Data are the moving average ± s.e.m. for <i>n</i> = 21 cells from 4 experiments. ***<i>P</i> < 0.001 for all comparisons at normalized cell length > 0.96. The <i>x</i> axis is discontinued between 0.25 and 0.75 to highlight differences at the cell edges. <b>n</b>, Confined migration speeds of SC versus <i>ARP3</i>/<i>ARPC4</i> double-knockdown cells (<i>n</i> = 90) from 3 experiments. For <b>e</b>, <b>g</b>, <b>j</b> and <b>n</b>, data are mean ± s.d. Unless otherwise indicated, statistical comparison was performed with respect to 0.77 cP. Statistical analysis was performed using Kruskal–Wallis tests followed by Dunn’s test (<b>a</b> and <b>n</b>), Mann–Whitney <i>U</i>-tests (BrM2 only) or unpaired <i>t</i>-tests after log-transformation (other cells) (<b>b</b>), unpaired <i>t</i>-tests (<b>e</b>, <b>g</b> and <b>j</b>) and two-way analysis of variance (ANOVA) followed by Šidák’s test (<b>h</b> and <b>m</b>). Scale bars, 250 μm (<b>c</b>), 50 μm (<b>d</b>), 25 µm (<b>f</b>, white), 3 µm (<b>f</b>, red), 10 µm (<b>h</b>), 2 µm (<b>i</b>), 20 µm (<b>l</b>). The cell model was MDA-MB-231 unless otherwise indicated. *<i>P</i> <i><</i> 0.05, **<i>P</i> <i><</i> 0.01, ***<i>P</i> <i><</i> 0.001, ****<i>P</i> < 0.0001. Credit: <i>Nature</i> (2022). DOI: 10.1038/s41586-022-05394-6"> <figure class="article-img"> <img src="https://scx1.b-cdn.net/csz/news/800a/2022/new-clue-discovered-fo.jpg" alt="发现了关于癌细胞如何以及为什么扩散的新线索gydF4y2Ba" title="Viscosity enhances cell migration and promotes an ARP2/3-mediated dense actin network at the leading edge. <b>a</b>,<b>b</b>, Speeds of MDA-MB-231 cells (<b>a</b>) and other indicated cell types (<b>b</b>) inside confining channels at prescribed viscosities. The red lines represent the median of ≥69 cells from ≥3 experiments. <b>c</b>, Cell trajectories on 2D collagen-coated surfaces after 10 h. <b>d</b>, Cells disseminating from 3D spheroids. <b>e</b>, The time required for the first cell dissociation from each spheroid (<i>n</i> ≥ 53) from 3 experiments. <b>f</b>, Airyscan images of phalloidin stained cells on collagen-coated substrates. The red arrow indicates high F-actin staining along the cell edge. <b>g</b>, The fraction of cell-projected area with a Lifeact–GFP-rich lamella for <i>n</i> ≥ 28 cells from 3 experiments. <b>h</b>, The leading edge of Lifeact–GFP-expressing cells on collagen-coated surfaces at <i>t</i> = 0 min (red) and <i>t</i> = 2 min (cyan) (left). Right, leading-edge lamella growth in <i>n</i> ≥ 19 cells from 3 experiments. Data are the moving average ± s.e.m. <i>P</i> < 0.05 for all points <i>t</i> ≥ 50 s. Time is shown as min:s. <b>i</b>,<b>j</b>, STORM reconstruction (<b>i</b>) and density quantification (<b>j</b>) of F-actin for cells (<i>n</i> ≥ 13) on substrates from 2 experiments. <b>k</b>, The average actin density over time from 20 stochastic simulations. Viscous forces were applied at <i>t</i> = 6 s (red arrow) and maintained until the end of the simulation. <b>l</b>, Confocal images of cells expressing Lifeact–GFP and ARP3–mCherry in confinement. The red arrow indicates high ARP3 intensity at leading-edge protrusions at 8 cP. <b>m</b>, The relative ARP3–mCherry intensity along normalized cell length in confined cells. Data are the moving average ± s.e.m. for <i>n</i> = 21 cells from 4 experiments. ***<i>P</i> < 0.001 for all comparisons at normalized cell length > 0.96. The <i>x</i> axis is discontinued between 0.25 and 0.75 to highlight differences at the cell edges. <b>n</b>, Confined migration speeds of SC versus <i>ARP3</i>/<i>ARPC4</i> double-knockdown cells (<i>n</i> = 90) from 3 experiments. For <b>e</b>, <b>g</b>, <b>j</b> and <b>n</b>, data are mean ± s.d. Unless otherwise indicated, statistical comparison was performed with respect to 0.77 cP. Statistical analysis was performed using Kruskal–Wallis tests followed by Dunn’s test (<b>a</b> and <b>n</b>), Mann–Whitney <i>U</i>-tests (BrM2 only) or unpaired <i>t</i>-tests after log-transformation (other cells) (<b>b</b>), unpaired <i>t</i>-tests (<b>e</b>, <b>g</b> and <b>j</b>) and two-way analysis of variance (ANOVA) followed by Šidák’s test (<b>h</b> and <b>m</b>). Scale bars, 250 μm (<b>c</b>), 50 μm (<b>d</b>), 25 µm (<b>f</b>, white), 3 µm (<b>f</b>, red), 10 µm (<b>h</b>), 2 µm (<b>i</b>), 20 µm (<b>l</b>). The cell model was MDA-MB-231 unless otherwise indicated. *<i>P</i> <i><</i> 0.05, **<i>P</i> <i><</i> 0.01, ***<i>P</i> <i><</i> 0.001, ****<i>P</i> < 0.0001. Credit: <i>Nature</i> (2022). DOI: 10.1038/s41586-022-05394-6" width="800" height="530"> <figcaption class="text-darken text-low-up text-truncate-js text-truncate mt-3"> 黏度增强细胞迁移，促进arp2 /3介导的致密肌动蛋白网络在前沿。<bgydF4y2Ba>一个</bgydF4y2Ba>，<bgydF4y2Ba>b</bgydF4y2Ba>， MDA-MB-231细胞的速度(<bgydF4y2Ba>一个</bgydF4y2Ba>)和其他指定的细胞类型(<bgydF4y2Ba>b</bgydF4y2Ba>)在规定粘度的封闭通道内。红线代表≥3次实验中≥69个细胞的中位数。<bgydF4y2Ba>c</bgydF4y2Ba>， 10 h后细胞在二维胶原蛋白表面的运动轨迹。<bgydF4y2Ba>d</bgydF4y2Ba>，细胞从三维球体播散。<bgydF4y2Ba>e</bgydF4y2Ba>，第一个细胞从每个球体分离所需的时间(<我>n</我>≥53)来自3个实验。<bgydF4y2Ba>f</bgydF4y2Ba>，胶原涂布基质上阴茎素染色细胞的airscan图像。红色箭头表示沿细胞边缘高f -肌动蛋白染色。<bgydF4y2Ba>g</bgydF4y2Ba>，富含lifeact - gfp薄片的细胞投影面积的比例<我>n</我>3个实验≥28个细胞。<bgydF4y2Ba>h</bgydF4y2Ba>，胶原蛋白涂层表面表达lifeact - gfp细胞的前沿<我>t</我>= 0 min(红色)和<我>t</我>= 2分钟(青色)(左)。右，前缘片层生长<我>n</我>3个实验≥19个细胞。数据为移动平均线±s.e.m。<我>P</我>所有得分均< 0.05<我>t</我>≥50s。时间以min:s表示。<bgydF4y2Ba>我</bgydF4y2Ba>，<bgydF4y2Ba>j</bgydF4y2Ba>， STORM重建(<bgydF4y2Ba>我</bgydF4y2Ba>)和密度量化(<bgydF4y2Ba>j</bgydF4y2Ba>)用于细胞的f -肌动蛋白(<我>n</我>≥13)。<bgydF4y2Ba>k</bgydF4y2Ba>， 20个随机模拟的平均肌动蛋白密度随时间的变化。施加粘性力<我>t</我>= 6秒(红色箭头)，并一直保持到模拟结束。<bgydF4y2Ba>l</bgydF4y2Ba>表达Lifeact-GFP和ARP3-mCherry细胞的共聚焦图像。红色箭头表示8 cP时前缘突出处的高ARP3强度。<bgydF4y2Ba>米</bgydF4y2Ba>，封闭细胞中ARP3-mCherry相对强度沿归一化细胞长度变化。数据为移动平均线±s.e.m。为<我>n</我>= 4个实验中的21个细胞。＊＊＊<我>P</我>在归一化细胞长度> 0.96的所有比较中< 0.001。的<我>x</我>Axis在0.25和0.75之间停止，以突出显示单元格边缘的差异。<bgydF4y2Ba>n</bgydF4y2Ba>， SC对的限制迁移速度<我>ARP3</我>/<我>ARPC4</我>双敲除细胞(<我>n</我>= 90)从3个实验。为<bgydF4y2Ba>e</bgydF4y2Ba>，<bgydF4y2Ba>g</bgydF4y2Ba>，<bgydF4y2Ba>j</bgydF4y2Ba>而且<bgydF4y2Ba>n</bgydF4y2Ba>，数据为均数±标准差。除非另有说明，以0.77 cP进行统计学比较。采用Kruskal-Wallis检验进行统计学分析，然后采用Dunn 's检验(<bgydF4y2Ba>一个</bgydF4y2Ba>而且<bgydF4y2Ba>n</bgydF4y2Ba>), Mann-Whitney<我>U</我>-tests(仅限BrM2)或未配对<我>t</我>-日志转换后的测试(其他单元格)(<bgydF4y2Ba>b</bgydF4y2Ba>),未配对<我>t</我>测试(<bgydF4y2Ba>e</bgydF4y2Ba>，<bgydF4y2Ba>g</bgydF4y2Ba>而且<bgydF4y2Ba>j</bgydF4y2Ba>)和双向方差分析(ANOVA)，然后是Šidák的检验(<bgydF4y2Ba>h</bgydF4y2Ba>而且<bgydF4y2Ba>米</bgydF4y2Ba>)．比例尺，250 μm (<bgydF4y2Ba>c</bgydF4y2Ba>)， 50 μm (<bgydF4y2Ba>d</bgydF4y2Ba>)， 25µm (<bgydF4y2Ba>f</bgydF4y2Ba>，白色)，3µm (<bgydF4y2Ba>f</bgydF4y2Ba>，红色)，10µm (<bgydF4y2Ba>h</bgydF4y2Ba>)， 2µm (<bgydF4y2Ba>我</bgydF4y2Ba>)， 20µm (<bgydF4y2Ba>l</bgydF4y2Ba>)．除非另有说明，细胞模型为MDA-MB-231。＊<我>P</我> <i><</我>0.05, * *<我>P</我> <i><</我>0.01, * * *<我>P</我> <i><</我>0.001, * * * *<我>P</我>< 0.0001。信贷:<我>自然</我>(2022)。DOI: 10.1038 / s41586 - 022 - 05394 - 6</f我gc一个ption> </figure> </div> </div> <p>一个国际研究小组发现了一种新的机制，使癌细胞能够在全身移动，为阻止转移提供了一个潜在的新靶点，90%的癌症死亡都是由转移造成的。</gydF4y2Bap> <div class="article-banner first-banner ads-336x280">  <div id="div-gpt-ad-1450190541376-1"></div> </div> <p>研究结果发表在<我>自然</我>研究小组发现，当癌细胞被较稠的液体包围时，它们移动得更快，这种变化发生在淋巴引流被原发肿瘤破坏时。</gydF4y2Bap> <p>“这真的是第一次<一个href="//www.puressens.com/tags/viscosity/" rel="tag" class="textTag">粘度</一个>亚伯达大学医学与牙科学院转化肿瘤学教授兼鸟狗教授约翰·d·刘易斯说。“现在我们知道液体粘度会给癌细胞发出特定的信号，让它们以特定的方式移动，我们可能会使用药物来切断这种信号<一个href="//www.puressens.com/tags/pathway/" rel="tag" class="textTag">通路</一个>并鼓励癌细胞减缓，甚至可能停止。”</gydF4y2Bap> <p>刘易斯实验室被邀请加入由约翰霍普金斯大学的研究人员领导的项目，因为它在利用受精卵的胎盘样绒毛尿囊膜实时成像人类癌细胞方面具有专长。</gydF4y2Bap> <p>刘易斯说:“我想说，我们是这类成像的世界领导者。”“我们对这项工作的贡献是非常精确地显示癌细胞改变了它们<一个href="//www.puressens.com/tags/gene+expression/" rel="tag" class="textTag">基因表达</一个>当它们遇到周围流体粘度增加时，就会变得更具攻击性。即使你把粘度降低了，这些细胞仍然更具攻击性。”</gydF4y2Bap> <p>Lewis说:“然后我们继续表明，当癌细胞中的这一信号通路受到干扰时，它会改变它们逃离血液和转移的能力。”</gydF4y2Bap> <p>这是该国际研究团队发表的第三篇论文。刘易斯将他的团队的大部分工作归功于高级研究助理康斯坦丁·斯托莱托夫。他警告说，一旦确定了新的治疗靶点，可能需要10到15年的时间来开发和测试一种药物。</gydF4y2Bap> <p>“但这有助于我们建立对如何做到这一点的理解<一个href="//www.puressens.com/tags/cancer+cells/" rel="tag" class="textTag">癌症细胞</一个>行动起来，这就增加了我们用整个方法取得成功的机会。”</gydF4y2Bap> <div class="article-main__more p-4"> <strong>更多信息:</gydF4y2Bastrong>Kaustav Bera等人，细胞外液粘度增强细胞迁移和癌症扩散，<我>自然</我>(2022)。<一个d一个t一个-doi="1" href="https://dx.doi.org/10.1038/s41586-022-05394-6" target="_blank">DOI: 10.1038 / s41586 - 022 - 05394 - 6</一个> <div class="mt-3"> <strong>期刊信息:</gydF4y2Bastrong> <a href="//www.puressens.com/journals/nature/"><cite>自然</c我te></a> <a class="icon_open" href="http://www.nature.com/nature/index.html" target="_blank" rel="nofollow"> <svg> <use href="https://medx.b-cdn.net/tmpl/v6/img/svg/sprite.svg#icon_open" x="0" y="0"></use> </svg></a> <p></p> </div> </div> <div class="d-inline-block text-medium my-4"> 所提供的<一个href="//www.puressens.com/partners/university-of-alberta/">阿尔伯塔大学</一个> <a class="icon_open" href="http://www.ualberta.ca/" target="_blank" rel="nofollow"> <svg> <use href="https://medx.b-cdn.net/tmpl/v6/img/svg/sprite.svg#icon_open" x="0" y="0"></use> </svg></a> </div>  <div class="d-none d-print-block"> <div class="mb-4"> <strong>引用</gydF4y2Bastrong>:关于癌细胞如何以及为什么扩散的新线索(2022,12月5日)于2022年12月8日从//www.puressens.com/news/2022-12-clue-cancer-cells.html检索</d我v> <div class="border text-muted p-3"> 这份文件受版权保护。除为私人学习或研究目的而进行的公平交易外，未经书面许可，不得转载任何部分。内容仅供参考之用。</d我v> </div> </div> </article> <hr> <div class="article-main__explore my-4 d-print-none"> <div class="d-flex align-items-center"> <svg> <use 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