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miR-155 contributes to the progression of glioma by enhancing Wnt/β-catenin pathway

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Tumor Biology

Abstract

As the most common brain tumor, glioma is featured with poor prognosis due to its resistance to current therapeutic strategies. The elucidation of etiology is believed to facilitate the development of novel effective anti-glioma treatment modalities. As a confirmed oncogenic microRNA (miRNA) in many other types of cancers, the role of miR-155 in glioma is still unknown. This study is aimed to study the role of miR-155 in the progression of glioma. Our results revealed that miR-155 was overexpressed in the collected glioma specimen, compared with noncancerous brain tissues. The suppression of miR-155 attenuated the proliferation of glioma cells and the activation of Wnt pathway. Silencing miR-155 was also able to suppress the growth of U-87 MG glioma xenografts in mice. Pearson analysis indicated that miR-155 level was inversely correlated with the abundance of HMG-box transcription factor 1 (HBP1), a strong Wnt pathway inhibitor, in glioma samples. Further experiments confirmed that miR-155 suppressed the expression of HBP1 by targeting the putative miRNA recognition elements (MREs) within its messenger RNA (mRNA) 3′ untranslated region (UTR). Furthermore, HBP1 small interfering RNA (siRNA) abolished the effect of miR-155 suppression on the proliferation of glioma and the activation of Wnt pathway. Taken together, miR-155 promoted the progression of glioma by enhancing the activation of Wnt pathway. Thus, targeting miR-155 may be an effective strategy for glioma treatment.

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Funding

This study was supported by the Research Award Fund for Outstanding Middle-aged and Young Scientists of Shandong Province, China (No. BS2011SW004 and the Scientific Research Fund for Excellent Youth in the Affiliated Hospital of Qingdao University (No. 201506).

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Correspondence to Qinghai Meng.

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Yan, Z., Che, S., Wang, J. et al. miR-155 contributes to the progression of glioma by enhancing Wnt/β-catenin pathway. Tumor Biol. 36, 5323–5331 (2015). https://doi.org/10.1007/s13277-015-3193-9

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  • DOI: https://doi.org/10.1007/s13277-015-3193-9

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