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Zhang J, Zhang J, Zhang J, et al. MicroRNA-625 inhibits the proliferation and increases the chemosensitivity of glioma by directly targeting AKT2. Am J Cancer Res. 2017;7(9):1835-1849
Zhang, J., Zhang, J., Zhang, J., Qiu, W., Xu, S., Yu, Q., Liu, C., Wang, Y., Lu, A., Zhang, J., & Lu, X. (2017). MicroRNA-625 inhibits the proliferation and increases the chemosensitivity of glioma by directly targeting AKT2. American journal of cancer research, 7(9), 1835-1849.
Zhang, Jiale, et al. "MicroRNA-625 inhibits the proliferation and increases the chemosensitivity of glioma by directly targeting AKT2." American journal of cancer research vol. 7,9 (2017): 1835-1849.
Zhang J, Zhang J, Zhang J, Qiu W, Xu S, Yu Q, Liu C, Wang Y, Lu A, Zhang J, Lu X. MicroRNA-625 inhibits the proliferation and increases the chemosensitivity of glioma by directly targeting AKT2. Am J Cancer Res. 2017 Sep 01;7(9):1835-1849. eCollection 2017. PMID: 28979807; PMCID: PMC5622219.
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Am J Cancer Res. 2017 Sep 01;7(9):1835-1849. eCollection 2017.

MicroRNA-625 inhibits the proliferation and increases the chemosensitivity of glioma by directly targeting AKT2.

American journal of cancer research

Jiale Zhang, Jian Zhang, Jie Zhang, Wenjin Qiu, Shuo Xu, Qun Yu, Chengke Liu, Yingyi Wang, Ailin Lu, Junxia Zhang, Xiaoming Lu

Affiliations

  1. Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University300 Guangzhou Road, Nanjing 210029, Jiangsu Province, People's Republic of China.
  2. Department of Neurosurgery, The Affiliated Hospital of Guizhou Medical University300 Guangzhou Road, Guiyang 550004, Guizhou Province, People's Republic of China.
  3. Department of Neurosurgery, Liyang Hospital of TCM121# Xihou Street, Liyang 213300, Jiangsu Province, People's Repubulic of China.

PMID: 28979807 PMCID: PMC5622219

Abstract

Glioma is a malignant tumor for which new therapies are needed. Growing evidence has demonstrated that microRNAs (miRNAs) have a major effect on glioma development. Here, we aimed to characterize a novel anti-cancer miRNA, miR-625, by investigating its expression, function, and mechanism of action in glioma progression. The expression of miR-625 and its target mRNA in human glioma tissues and cell lines was assessed by real-time PCR, western blotting, and immunohistochemistry. Functional significance was assessed by examining cell cycle progression, proliferation, apoptosis, and chemosensitivity to temozolomide in vitro, and by examining growth of subcutaneous glioblastoma in a mouse model in vivo. We found that miR-625 expression was significantly lower in human glioma samples and cell lines than in normal brain tissue and human astrocytes. Furthermore, miR-625 overexpression not only suppressed glioma cell proliferation in culture and in the tumor xenograft model but also induced cell cycle arrest and apoptosis. AKT2 was identified as a direct miR-625 target in glioma cell lines, and AKT2 overexpression reversed the suppressive effects of miR-625 in the cell lines and the tumor xenograft model. Finally, we found that the sensitivity of glioma cells to temozolomide was increased by miR-625 overexpression, and this was reversed by concomitant AKT2 expression. In conclusion, our findings suggest that the miR-625-AKT2 axis could be a new prognostic marker and diagnostic target for gliomas.

Keywords: AKT2; Glioma; miR-625; proliferation

Conflict of interest statement

None.

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