Liu Huayang, Dowdle James A, Khurshid Safiya, Sullivan Nicholas J, Bertos Nicholas, Rambani Komal, Mair Markus, Daniel Piotr, Wheeler Esther, Tang Xing, Toth Kyle, Lause Michael, Harrigan Markus E, Eiring Karl, Sullivan Connor, Sullivan Matthew J, Chang Serena W, Srivastava Siddhant, Conway Joseph S, Kladney Raleigh, McElroy Joseph, Bae Sooin, Lu Yuanzhi, Tofigh Ali, Saleh Sadiq M I, Fernandez Soledad A, Parvin Jeffrey D, Coppola Vincenzo, Macrae Erin R, Majumder Sarmila, Shapiro Charles L, Yee Lisa D, Ramaswamy Bhuvaneswari, Hallett Michael, Ostrowski Michael C, Park Morag, Chamberlin Helen M, Leone Gustavo
Solid Tumor Biology Program, Comprehensive Cancer Center, The Ohio State University, Columbus, OH 43210, USA; Department of Molecular Genetics, The Ohio State University, 484 West 12th Avenue, Columbus, OH 43210, USA; Department of Cancer Biology and Genetics, McGill University, Montreal, QC H3A 1A1, Canada.
Department of Biochemistry, Rosalind and Morris Goodman Cancer Center, McGill University, Montreal, QC H3A 1A1, Canada; Department of Oncology, McGill University, Montreal, QC H3A 1A1, Canada.
Dev Cell. 2017 May 22;41(4):392-407.e6. doi: 10.1016/j.devcel.2017.04.024.
Mesodermal cells signal to neighboring epithelial cells to modulate their proliferation in both normal and disease states. We adapted a Caenorhabditis elegans organogenesis model to enable a genome-wide mesodermal-specific RNAi screen and discovered 39 factors in mesodermal cells that suppress the proliferation of adjacent Ras pathway-sensitized epithelial cells. These candidates encode components of protein complexes and signaling pathways that converge on the control of chromatin dynamics, cytoplasmic polyadenylation, and translation. Stromal fibroblast-specific deletion of mouse orthologs of several candidates resulted in the hyper-proliferation of mammary gland epithelium. Furthermore, a 33-gene signature of human orthologs was selectively enriched in the tumor stroma of breast cancer patients, and depletion of these factors from normal human breast fibroblasts increased proliferation of co-cultured breast cancer cells. This cross-species approach identified unanticipated regulatory networks in mesodermal cells with growth-suppressive function, exposing the conserved and selective nature of mesodermal-epithelial communication in development and cancer.
在正常和疾病状态下,中胚层细胞都会向邻近的上皮细胞发出信号,以调节其增殖。我们采用了一种秀丽隐杆线虫器官发生模型,进行全基因组中胚层特异性RNA干扰筛选,发现中胚层细胞中有39个因子可抑制相邻的Ras信号通路敏感上皮细胞的增殖。这些候选因子编码蛋白质复合物和信号通路的组成部分,它们共同控制染色质动态、细胞质多聚腺苷酸化和翻译。对几种候选因子的小鼠直系同源基因进行基质成纤维细胞特异性缺失,导致乳腺上皮细胞过度增殖。此外,人类直系同源基因的一个33基因特征在乳腺癌患者的肿瘤基质中选择性富集,从正常人乳腺成纤维细胞中去除这些因子会增加共培养的乳腺癌细胞的增殖。这种跨物种方法在具有生长抑制功能的中胚层细胞中发现了意想不到的调控网络,揭示了中胚层-上皮细胞在发育和癌症中的通讯的保守性和选择性。