miR-23a acts as an oncogene in pancreatic carcinoma by targeting FOXP2

MicroRNAs have been reported to play an important role in tumor development and progression by targeting oncogenes and tumor suppressors. miR-23a has been described as significantly upregulated in multiple cancers and involved in tumorigenesis. The aim of this study was to evaluate the potential rol...

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Bibliographic Details
Published in:Journal of investigative medicine 2018-03, Vol.66 (3), p.676-683
Main Authors: Diao, Hongliang, Ye, Zhou, Qin, Renyi
Format: Article
Language:English
Subjects:
Adult
Aged
Apoptosis
Base Sequence
Biomarkers
Bone cancer
Cancer therapies
Cell growth
Cell Line, Tumor
Cell Proliferation - genetics
Female
Forkhead Transcription Factors - genetics
Forkhead Transcription Factors - metabolism
Gene Expression Regulation, Neoplastic
Humans
Lung cancer
Male
Medical prognosis
Metastasis
MicroRNAs
MicroRNAs - genetics
MicroRNAs - metabolism
Middle Aged
Neoplasm Invasiveness
Oncogenes
Pancreatic cancer
Pancreatic Neoplasms
Pancreatic Neoplasms - genetics
Pancreatic Neoplasms - pathology
Proteins
Tumorigenesis
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Summary:MicroRNAs have been reported to play an important role in tumor development and progression by targeting oncogenes and tumor suppressors. miR-23a has been described as significantly upregulated in multiple cancers and involved in tumorigenesis. The aim of this study was to evaluate the potential roles of miR-23a in pancreatic ductal adenocarcinoma (PDAC). We found that miR-23a level was significantly increased in tissues of PDAC compared with that in the control by real-time PCR. FOXP2 expression was downregulated and inversely correlated with miR-23a. miR-23a directly targeted the 3’-untranslated region of FOXP2 mRNA and repressed its expression. Mechanistically, enhancement of miR-23a by transfection with mimics in Aspc-1 cells significantly promoted cell proliferation and invasion, while miR-23a inhibitors transfection in SW1990 cells induced an inhibitory effect. Moreover, restoration of FOXP2 impaired the pro-proliferation and proinvasion effects of miR-23a, indicating FOXP2 is a direct mediator of miR-23a functions. In conclusion, our findings suggest a novel miR-23a/FOXP2 link contributing to PDAC development and invasion. It may be a potential diagnostic and therapeutic target for PDAC.
ISSN:1081-5589
1708-8267
DOI:10.1136/jim-2017-000598