Endogenous Myc maintains the tumor microenvironment

被引:159
作者
Sodir, Nicole M. [1 ,2 ]
Swigart, Lamorna Brown [1 ,2 ]
Karnezis, Anthony N. [1 ,2 ]
Hanahan, Douglas [3 ]
Evan, Gerard I. [1 ,2 ,4 ]
Soucek, Laura [1 ,2 ]
机构
[1] Univ Calif San Francisco, Dept Pathol, San Francisco, CA 94143 USA
[2] Univ Calif San Francisco, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA 94143 USA
[3] Ecole Polytech Fed Lausanne, Swiss Fed Inst Technol, Swiss Inst Expt Canc Res, CH-1015 Lausanne, Switzerland
[4] Univ Cambridge, Dept Biochem, Cambridge CB2 1GA, England
关键词
Myc inhibition; pancreas; tumor; microenvironment; therapeutics; MATRIX-METALLOPROTEINASE INHIBITORS; ANGIOGENIC SWITCH; CANCER-THERAPY; T-ANTIGEN; EXPRESSION; RESISTANCE; INDUCTION; TRIGGERS; OMOMYC; CELLS;
D O I
10.1101/gad.2038411
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
The ubiquitous deregulation of Myc in human cancers makes it an intriguing therapeutic target, a notion supported by recent studies in Ras-driven lung tumors showing that inhibiting endogenous Myc triggers ubiquitous tumor regression. However, neither the therapeutic mechanism nor the applicability of Myc inhibition to other tumor types driven by other oncogenic mechanisms is established. Here, we show that inhibition of endogenous Myc also triggers ubiquitous regression of tumors in a simian virus 40 (SV40)-driven pancreatic islet tumor model. Such regression is presaged by collapse of the tumor microenvironment and involution of tumor vasculature. Hence, in addition to its diverse intracellular roles, endogenous Myc serves an essential and nonredundant role in coupling diverse intracellular oncogenic pathways to the tumor microenvironment, further bolstering its credentials as a pharmacological target.
引用
收藏
页码:907 / 916
页数:10
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