YTH domain family 2 orchestrates epithelial-mesenchymal transition/proliferation dichotomy in pancreatic cancer cells

Recent studies show that YTH domain family 2 (YTHDF2) preferentially binds to m A-containing mRNA regulates localization and stability of the bound mRNA. However, the role of YTHDF2 in pancreatic cancers remains to be elucidated. Here, we find that YTHDF2 expression is up-regulated in pancreatic can...

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Bibliographic Details
Published in:	Cell cycle (Georgetown, Tex.) Vol. 16; no. 23; pp. 2259 - 2271
Main Authors:	Chen, Jixiang, Sun, Yaocheng, Xu, Xiao, Wang, Dawei, He, Junbo, Zhou, Hailang, Lu, Ying, Zeng, Jian, Du, Fengyi, Gong, Aihua, Xu, Min
Format:	Journal Article
Language:	English
Published:	United States Taylor & Francis 01.01.2017
Subjects:	Adaptor Proteins, Signal Transducing - metabolism Cell Line, Tumor Cell Movement Cell Proliferation Epithelial-Mesenchymal Transition G1 Phase Cell Cycle Checkpoints Humans Neoplasm Staging Pancreatic Neoplasms - metabolism Pancreatic Neoplasms - pathology Phosphoproteins - metabolism Proto-Oncogene Proteins c-akt - metabolism RNA Interference RNA, Small Interfering - metabolism RNA-Binding Proteins - antagonists & inhibitors RNA-Binding Proteins - genetics RNA-Binding Proteins - metabolism Signal Transduction Smad Proteins - metabolism Transcription Factors Transforming Growth Factor beta - metabolism Up-Regulation YAP pancreatic cancer YTHDF2 migration-proliferation dichotomy EMT
ISSN:	1538-4101, 1551-4005, 1551-4005
Online Access:	Get full text
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Summary:	Recent studies show that YTH domain family 2 (YTHDF2) preferentially binds to m A-containing mRNA regulates localization and stability of the bound mRNA. However, the role of YTHDF2 in pancreatic cancers remains to be elucidated. Here, we find that YTHDF2 expression is up-regulated in pancreatic cancer tissues compared with normal tissues at both mRNA and protein levels, and is higher in clinical patients with later stages of pancreatic cancer, indicating that YTHDF2 possesses potential clinical significance for diagnosis and prognosis of pancreatic cancers. Furthermore, we find that YTHDF2 orchestrates two cellular processes: promotes proliferation and inhibits migration and invasion in pancreatic cancer cells, a phenomenon called "migration-proliferation dichotomy", as well as epithelial-mesenchymal transition (EMT) in pancreatic cancer cells. Furthermore, YTHDF2 knockdown significantly increases the total YAP expression, but inhibits TGF-β/Smad signaling, indicating that YTHDF2 regulates EMT probably via YAP signaling. In summary, all these findings suggest that YTHDF2 may be a new predictive biomarker of development of pancreatic cancer, but a serious consideration is needed to treat YTHDF2 as a target for pancreatic cancer.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Supplemental data for this article can be accessed on the publisher's website. These authors contributed equally to this work.
ISSN:	1538-4101 1551-4005 1551-4005
DOI:	10.1080/15384101.2017.1380125