Oncotarget

Research Papers:

MiR-19 regulates the proliferation and invasion of glioma by RUNX3 via β-catenin/Tcf-4 signaling

Jikui Sun, Zhifan Jia, Banban Li, Anling Zhang, Guangxiu Wang, Peiyu Pu, Zhijuan Chen, Zengguang Wang and Weidong Yang _

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Oncotarget. 2017; 8:110785-110796. https://doi.org/10.18632/oncotarget.22720

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Abstract

Jikui Sun1,*, Zhifan Jia2,*, Banban Li3,*, Anling Zhang2, Guangxiu Wang2, Peiyu Pu2, Zhijuan Chen2, Zengguang Wang2 and Weidong Yang2

1Department of Neurosurgery, Affiliated Hospital of Taishan Medical University, Life Science Research Center of Taishan Medical University, Taian, 271000, P.R. China

2Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin Neurological Institute, Key Laboratory of Post-trauma Neuro-repair and Regeneration in Central Nervous System, Ministry of Education, Tianjin Key Laboratory of Injuries, Variations and Regeneration of Nervous System, Tianjin, 300052, P.R. China

3Department of Hematopathology, Affiliated Taishan Hospital of Taishan Medical University, Taian, 271000, P.R. China

*These authors contributed equally to this work

Correspondence to:

Weidong Yang, email: weidongyang16@163.com

Keywords: miR-19; RUNX3; β-catenin; TCF4; glioma

Received: June 22, 2017     Accepted: October 28, 2017     Published: November 28, 2017

ABSTRACT

Accumulating data demonstrates that the network dysregulation of microRNA-medicated target genes is involved in glioma. We have previously found miR-19a/b overexpression in glioma cell lines and specimens with various tumour grades. However, there was no report on the function and regulatory mechanism of miR-19a/b in glioma. In this study, based on our previous research data, we first determine the inverse relationship between miR-19 (miR-19a and miR-19b) and RUNX3 which is also identified the reduced expression in tumour tissues by real-time PCR and IHC. Luciferase reporter assay and western blot analysis revealed that RUNX3 was a direct target of miR-19. Down-regulation of miR-19 dramatically inhibited proliferation, invasion and induced the cell cycle G1 arrest and apoptosis, at least partly via the up-regulation of RUNX3. Furthermore, Mechanistic investigation indicated that knockdown of miR-19 repressed the β-catenin/TCF4 transcription activity. In conclusion, our study validates a pathogenetic role of miR-19 in glioma and establishes a potentially regulatory and signaling involving miR-19 /RUNX3/β-catenin, also suggesting miR-19 may be a candidate therapeutic target in glioma.


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