High level of miR-221/222 confers increased cell invasion and poor prognosis in glioma View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2012-12

AUTHORS

Chunzhi Zhang, Junxia Zhang, Jianwei Hao, Zhendong Shi, Yingyi Wang, Lei Han, Shizhu Yu, Yongping You, Tao Jiang, Jinhuan Wang, Meili Liu, Peiyu Pu, Chunsheng Kang

ABSTRACT

BACKGROUND: MiR-221 and miR-222 (miR-221/222), upregulated in gliomas, can regulate glioma cell cycle progression and apoptosis, respectively. However, the association of miR-221/222 with glioma cell invasion and survival remains unknown. METHODS: Invasion capability of miR-221/222 was detected by mutiple analyses, including diffusion tensor imaging (DTI), transwell, wound healing and nude mouse tumor xenograft model assay. Further, the target of miR-221/222 was determined by luciferase reporter, western blot and gene rescue assay. The association of miR-221/222 with outcome was examined in fifty glioma patients. RESULTS: MiR-221/222 expression was significantly increased in high-grade gliomas compared with low-grade gliomas, and positively correlated with the degree of glioma infiltration. Over-expression of miR-221/222 increased cell invasion, whereas knockdown of miR-221/222 decreased cell invasion via modulating the levels of the target, TIMP3. Introduction of a TIMP3 cDNA lacking 3' UTR abrogated miR-221/222-induced cell invasion. In addition, knockdown of miR-221/222 increased TIMP3 expression and considerably inhibited tumor growth in a xenograft model. Finally, the increased level of miR-221/222 expression in high-grade gliomas confers poorer overall survival. CONCLUSIONS: The present data indicate that miR-221 and miR-222 directly regulate cell invasion by targeting TIMP3 and act as prognostic factors for glioma patients. More... »

PAGES

119

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/1479-5876-10-119

DOI

http://dx.doi.org/10.1186/1479-5876-10-119

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1008665111

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/22681957


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