期刊
CANCER RESEARCH
卷 77, 期 1, 页码 100-111出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-16-1898
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资金
- National Natural Science Foundation of China [31325008, 91640201, 91419307, 31300656, 31270840]
- Ministry of Science and Technology of China [2014CB943103, 2014CB964802, 2012CB910803]
- Science and Technology Commission of Shanghai Municipality [13ZR1464300, 16XD1404900]
- Chinese Academy of Sciences [KJZD-EW-L01-2, 2013KIP202, XDB19010202]
KRAS activation occurring in more than 90% of pancreatic ductal adenocarcinomas (PDAC) drives progression and metastasis, but the underlying mechanisms involved in these processes are still poorly understood. Here, we show how KRAS acts through inflammatory NF-B-k signaling to activate the transcription factor YY1, which represses expression of the tumor suppressor gene miR-489. In PDAC cells, repression of miR-489 by KRAS signaling inhibited migration and metastasis by targeting the extracellular matrix factors ADAM9 and MMP7. miR-489 downregulation elevated levels of ADAM9 and MMP7, thereby enhancing the migration and metastasis of PDAC cells. Together, our results establish a pivotal mechanism of PDAC metastasis and suggest miR-489 as a candidate therapeutic target for their attack. (C) 2016 AACR.
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