Long noncoding RNA MEG3 inhibits proliferation and migration but induces autophagy by regulation of Sirt7 and PI3K/AKT/mTOR pathway in glioma cells

In our study, human glioblastoma U251 cells were used to explore the roles of MEG3 in glioma in vitro. Herein, the alterations of cell proliferation, migration, apoptosis, and autophagy in cells aberrantly expressing MEG3 were investigated. Moreover, the underlying mechanisms involving in the PI3K/AKT/mTOR pathway were also explored. AbstractGlioma is a common primary brain tumor with high mortality rate and poor prognosis. Long noncoding RNA maternally expressed gene 3 (MEG3) is a tumor suppressor in diverse cancer types. However, the role of MEG3 in glioma remains unclear. We aimed to explore the effects of MEG3 on U251 cells as well as the underlying mechanisms. U251 cells were stably transfected with different recombined plasmids to overexpress or silence MEG3. Effects of aberrantly expressed MEG3 on cell viability, migration, apoptosis, expressions of apoptosis ‐associated and autophagy‐associated proteins, and phosphorylated levels of key kinases in the PI3K/AKT/mTOR pathway were all evaluated. Then, messenger RNA (mRNA) and protein expression of Sirt7 in cells abnormally expressing MEG3 were estimated. In addition, effects of abnormally expressed MEG 3 and Sirt7 on U251 cells were determined to reveal the underlying mechanism of MEG3‐associated modulation. Cell viability and migration were significantly reduced by MEG3 overexpression whereas cell apoptosis as well as Bax and cleaved caspase‐3/‐9 proteins were obviously induced. Beclin‐1 and LC3‐II/LC3‐I...
Source: Journal of Cellular Biochemistry - Category: Biochemistry Authors: Tags: RESEARCH ARTICLE Source Type: research