MicroRNA-1908 functions as a glioblastoma oncogene by suppressing PTEN tumor suppressor pathway.

Abstract

BACKGROUND:

We aimed to investigate whether miRNA-1908 is an oncogene in human glioblastoma and find the possible mechanism of miR-1908.

METHODS:

We investigated the growth potentials of miRNA-1908-overexpressing SW-1783 cells in vitro and in vivo. In order to identify the target molecule of miRNA-1908, a luciferase reporter assay was performed, and the corresponding downstream signaling pathway was examined using immunohistochemistry of human glioblastoma tissues. We also investigated the miRNA-1908 expression in 34 patients according to the postoperative risk of recurrence.

RESULTS:

The overexpression of miRNA-1908 significantly promoted anchorage-independent growth in vitro and significantly increased the tumor forming potential in vivo. MiRNA-1908 significantly suppressed the luciferase activity of mRNA combined with the PTEN 3'-UTR. Furthermore, the expression levels of miRNA-1908 were significantly increased in the patients with a high risk of recurrence compared to that observed in the low-risk patients, and this higher expression correlated with a poor survival.

CONCLUSIONS:

miRNA-1908 functions as an oncogene in glioblastoma by repressing the PTEN pathway. MiR-1908 is a potential new molecular marker for predicting the risk of recurrence and prognosis of glioblastoma.

• Authors: Xuewei Xia, Yong Li, Wenbo Wang, Fang Tang, Jie Tan, Liyuan Sun, Qinghua Li, Li Sun, Bo Tang, Songqing He
• Journal: Molecular cancer (Mol Cancer) Vol. 14 Pg. 154 (Aug 12 2015) ISSN: 1476-4598 [Electronic] England
• PMID: 26265437 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• MIRN1908 microRNA, human
• MicroRNAs
• Tumor Suppressor Proteins
• PTEN Phosphohydrolase

Topics

• Adult
• Aged
• Animals
• Brain Neoplasms (genetics, metabolism)
• Cell Line, Tumor
• Disease Models, Animal
• Female
• Gene Expression Regulation, Neoplastic
• Glioblastoma (genetics, metabolism, mortality, pathology, therapy)
• Heterografts
• Humans
• Male
• MicroRNAs (genetics)
• Middle Aged
• Oncogenes (genetics)
• PTEN Phosphohydrolase (genetics, metabolism)
• Prognosis
• Signal Transduction
• Tumor Suppressor Proteins (genetics, metabolism)