每时每刻，人体内成千上万的细胞在不停的移动，尤其是免疫反应、创伤修复等过程中。细胞迁移过程发生错误可造成肿瘤的形成和癌细胞的扩散。最近加州理工学院的研究人员利用线虫对细胞迁移的过程进行了深入研究，相关论文发表在PNAS上。

文章的通讯作者Paul Sternberg教授说，我们知道如何找到原发肿瘤，知道癌细胞何时扩散，但却对细胞何时迁移不清楚。Sternberg已对秀丽隐杆线虫（Caenorhabditis elegans）进行过多年的研究，尽管秀丽隐杆线虫的体型很小，却与人类有着很多相同的基因。

共同作者Mihoko Kato说，细胞迁移是一个非常保守的过程，因此无论发生在线虫或哺乳动物还是人中，我们都认为参与此过程的是一群相同的基因。

人或线虫的细胞中都有成千上万个基因，每个基因都有特定的功能，它们中约1/3比较活跃。为找到在细胞迁移过程中表达的基因，研究者以线虫体内一种名叫linker cell （LC）的细胞为研究对象，因为在线虫发育过程中，LC细胞的迁移基本跨越了整个线虫的长度。

利用高性能的显微镜，在相隔12小时的两个时间点，研究者观察并分离了幼虫的LC细胞，而后根据测序结果和计算分析找出在这两个迁移时间点高表达的基因。这种方法叫做transc**tional profiling，优点是可以使用任何细胞。

研究人员选择线虫和人共有的基因，如果发现某个基因在线虫细胞迁移中发挥作用，那么可以认为它在人体中也有助细胞迁移。

对细胞迁移进行深入研究有助于开发阻止这一过程的特定基因靶向的药物。进一步的研究中，研究人员希望找到迁移细胞的分子标记，进而为诊断提供便利。这项工作为找到癌细胞扩散的分子机制奠定了基础。

编译自：New insight into complexities of cell migration

Functional transc**tomics of a migrating cell in Caenorhabditis elegans

Erich M. Schwarza,b,1, Mihoko Katoa,b,1, and Paul W. Sternberg

In both metazoan development and metastatic cancer, migrating cells must carry out a detailed, complex program of sensing cues, binding substrates, and moving their cytoskeletons. The linker cell in Caenorhabditis elegans males undergoes a stereotyped migration that guides gonad organogenesis, occurs with precise timing, and requires the nuclear hormone receptor NHR-67. To better understand how this occurs, we performed RNA-seq of individually staged and dissected linker cells, comparing transc**tomes from linker cells of third-stage （L3） larvae, fourth-stage （L4） larvae, and nhr-67-RNAi–treated L4 larvae. We observed expression of 8,000–10,000 genes in the linker cell, 22–25% of which were up- or down-regulated 20-fold during development by NHR-67. Of genes that we tested by RNAi, 22% （45 of 204） were required for normal shape and migration, suggesting that many NHR-67–dependent, linker cell-enriched genes play roles in this migration. One unexpected class of genes up-regulated by NHR-67 was tandem pore potassium channels, which are required for normal linker-cell migration. We also found phenotypes for genes with human orthologs but no previously described migratory function. Our results provide an extensive catalog of genes that act in a migrating cell, identify unique molecular functions involved in nematode cell migration, and suggest similar functions in humans.