PURPOSE

Aberrant expression of long noncoding RNAs plays a pivotal role in tumorigenesis. Recently, several studies have showed that the LINC00152 gene is upregulated in a variety of tumors and plays an oncogene role; however, its underlying molecular mechanisms in glioblastoma remain unclear. In this study, we prepare to investigate the biological role and underlying molecular mechanisms of LINC00152 in glioblastoma cells.

METHODS

Bioinformatics analysis to identify LINC00152 expression, Cell Counting kit-8 assay and Colony formation assay were used to evaluate proliferation, Flow cytometric analysis was used to evaluate apoptosis, Cell Matrigel invasion assay and Wound healing assay was used to evaluate invasion, Western blot analysis to check protein expression level, Mouse xenograft models was used to check cell proliferation in vivo.

RESULTS

In this study, we found that LINC00152 was upregulated in gliomas and its expression was significantly associated with high tumor aggressiveness and poor outcomes for glioma patients. Functionally, the knockdown of LINC00152 not only inhibited malignant behaviors of glioma, such as proliferation and invasion of glioma cells and induced apoptosis in vitro but also suppressed tumorigenesis in vivo. Mechanistically, results of the bioinformatics analysis and experimental studies confirmed that LINC00152 and RAB10 as the targets of miR-107, and LINC00152 might act as a sponge for miR-107 to regulate the expression of RAB10 in glioblastoma. Additionally, silencing miR-107 reversed the effects induced by LINC00152 knockdown on glioblastoma cells both in vitro and in vivo.

CONCLUSION

Our data suggested that LINC00152 is a candidate prognostic marker of glioma, and that the LINC00152/MIR-107/RAB10 axis plays a pivotal role in regulation of the glioma malignancy, and therefore, targeting the axis might be an effective therapeutic strategy to treat glioma.