Oncogenic cooperation between SOCS family proteins and EGFR identified using a Drosophila epithelial transformation model

被引:67
作者
Herranz, Hector [1 ]
Hong, Xin [1 ,2 ]
Nguyen Thanh Hung [3 ]
Voorhoeve, P. Mathijs [3 ,4 ]
Cohen, Stephen M. [1 ,2 ]
机构
[1] Inst Mol & Cell Biol, Singapore 138673, Singapore
[2] Natl Univ Singapore, Dept Biol Sci, Singapore 119613, Singapore
[3] Duke NUS Natl Univ Singapore, Grad Sch Med, Singapore 169857, Singapore
[4] Natl Univ Singapore, Dept Biochem, Singapore 119613, Singapore
关键词
microRNA; cell proliferation; apoptosis; growth control; cancer; GROWTH-FACTOR RECEPTOR; CYTOKINE SIGNALING SOCS; CELL-PROLIFERATION; BANTAM MICRORNA; TUMOR-GROWTH; JAK/STAT; CANCER; EXPRESSION; SUPPRESSORS; REPRESSION;
D O I
10.1101/gad.192021.112
中图分类号
Q2 [细胞生物学];
学科分类号
071013 [干细胞生物学];
摘要
MicroRNAs (miRNAs) are emerging as cooperating factors that promote the activity of oncogenes in tumor formation and disease progression. This poses the challenge of identifying the miRNA targets responsible for these interactions. In this study, we identify the growth regulatory miRNA bantam and its target, Socs36E, as cooperating factors in EGFR-driven tumorigenesis and metastasis in a Drosophila model of epithelial transformation. bantam promotes growth by limiting expression of Socs36E, which functions as a negative growth regulator. Socs36E has only a modest effect on growth on its own, but behaves as a tumor suppressor in combination with EGFR activation. The human ortholog of SOCS36E, SOCS5, behaves as a candidate tumor suppressor in cellular transformation in cooperation with EGFR/RAS pathway activation.
引用
收藏
页码:1602 / 1611
页数:10
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