Kohn Kurt W, Zeeberg Barry M, Reinhold William C, Pommier Yves
Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, United States of America.
PLoS One. 2014 Jun 18;9(6):e99269. doi: 10.1371/journal.pone.0099269. eCollection 2014.
Using gene expression data to enhance our knowledge of control networks relevant to cancer biology and therapy is a challenging but urgent task. Based on the premise that genes that are expressed together in a variety of cell types are likely to functions together, we derived mutually correlated genes that function together in various processes in epithelial-like tumor cells. Expression-correlated genes were derived from data for the NCI-60 human tumor cell lines, as well as data from the Broad Institute's CCLE cell lines. NCI-60 cell lines that selectively expressed a mutually correlated subset of tight junction genes served as a signature for epithelial-like cancer cells. Those signature cell lines served as a seed to derive other correlated genes, many of which had various other epithelial-related functions. Literature survey yielded molecular interaction and function information about those genes, from which molecular interaction maps were assembled. Many of the genes had epithelial functions unrelated to tight junctions, demonstrating that new function categories were elicited. The most highly correlated genes were implicated in the following epithelial functions: interactions at tight junctions (CLDN7, CLDN4, CLDN3, MARVELD3, MARVELD2, TJP3, CGN, CRB3, LLGL2, EPCAM, LNX1); interactions at adherens junctions (CDH1, ADAP1, CAMSAP3); interactions at desmosomes (PPL, PKP3, JUP); transcription regulation of cell-cell junction complexes (GRHL1 and 2); epithelial RNA splicing regulators (ESRP1 and 2); epithelial vesicle traffic (RAB25, EPN3, GRHL2, EHF, ADAP1, MYO5B); epithelial Ca(+2) signaling (ATP2C2, S100A14, BSPRY); terminal differentiation of epithelial cells (OVOL1 and 2, ST14, PRSS8, SPINT1 and 2); maintenance of apico-basal polarity (RAB25, LLGL2, EPN3). The findings provide a foundation for future studies to elucidate the functions of regulatory networks specific to epithelial-like cancer cells and to probe for anti-cancer drug targets.
利用基因表达数据来增进我们对与癌症生物学和治疗相关的调控网络的了解是一项具有挑战性但又紧迫的任务。基于在多种细胞类型中共同表达的基因可能共同发挥作用这一前提,我们推导了在上皮样肿瘤细胞的各种过程中共同发挥作用的相互关联基因。表达相关基因来自NCI - 60人类肿瘤细胞系的数据以及布罗德研究所CCLE细胞系的数据。选择性表达紧密连接基因相互关联子集的NCI - 60细胞系用作上皮样癌细胞的一个特征标志。那些特征细胞系作为种子来推导其他相关基因,其中许多基因具有各种其他上皮相关功能。文献调查得出了关于那些基因的分子相互作用和功能信息,据此组装了分子相互作用图谱。许多基因具有与紧密连接无关的上皮功能,这表明引出了新的功能类别。相关性最高的基因涉及以下上皮功能:紧密连接处的相互作用(CLDN7、CLDN4、CLDN3、MARVELD3、MARVELD2、TJP3、CGN、CRB3、LLGL2、EPCAM、LNX1);黏着连接处的相互作用(CDH1、ADAP1、CAMSAP3);桥粒处的相互作用(PPL、PKP3、JUP);细胞 - 细胞连接复合体的转录调控(GRHL1和2);上皮RNA剪接调节因子(ESRP1和2);上皮小泡运输(RAB25、EPN3、GRHL2、EHF、ADAP1、MYO5B);上皮Ca(+2)信号传导(ATP2C2、S100A14、BSPRY);上皮细胞的终末分化(OVOL1和2、ST14、PRSS8、SPINT1和2);顶 - 基极性的维持(RAB25、LLGL2、EPN3)。这些发现为未来研究阐明上皮样癌细胞特有的调控网络功能以及探索抗癌药物靶点提供了基础。