Research Papers:

Dissecting dysfunctional crosstalk pathways regulated by miRNAs during glioma progression

Yunpeng Zhang, Yanjun Xu, Feng Li, Xiang Li, Li Feng, Xinrui Shi, Lihua Wang and Xia Li _

PDF  |  HTML  |  How to cite

Oncotarget. 2016; 7:25769-25782. https://doi.org/10.18632/oncotarget.8265

Metrics: PDF 1630 views  |   HTML 1817 views  |   ?  


Yunpeng Zhang1,*, Yanjun Xu1,*, Feng Li1, Xiang Li1, Li Feng1, Xinrui Shi1, Lihua Wang2, Xia Li1

1College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China

2Department of Neurology, The Second Affiliated Hospital, Harbin Medical University, Harbin 150081, China

*These authors have contributed equally to this work

Correspondence to:

Xia Li, e-mail: [email protected]

Lihua Wang, e-mail: [email protected]

Keywords: miRNAs, pathway crosstalk, glioma progression

Received: September 29, 2015     Accepted: March 08, 2016     Published: March 22, 2016


Glioma is a malignant nervous system tumor with a high fatality rate and poor prognosis. MicroRNAs (miRNAs) are important post-transcriptional modulators of glioma initiation and progression. Tumor progression often results from dysfunctional co-operation between pathways regulated by miRNAs. We therefore constructed a glioma progression-related miRNA-pathway crosstalk network that not only revealed some key miRNA-pathway patterns, but also helped characterize the functional roles of miRNAs during glioma progression. Our data indicate that crosstalk between cell cycle and p53 pathways is associated with grade II to grade III progression, while cell communications-related pathways involving regulation of actin cytoskeleton and adherens junctions are associated with grade IV glioblastoma progression. Furthermore, miRNAs and their crosstalk pathways may be useful for stratifying glioma and glioblastoma patients into groups with short or long survival times. Our data indicate that a combination of miRNA and pathway crosstalk information can be used for survival prediction.

Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 8265