Knockdown of PRR11 Induces Autophagy in Glioma Cells by Inhibiting Akt/mTOR Signaling Pathway

Glioma is the most common type of primary craniocerebral tumor. Understanding the molecular mechanisms of glioma occurrence and development will provide strategies for effectively treating glioma. Proline-rich protein 11 (PRR11) is a protein which is widely overexpressed in different tumors. TCGA data analysis showed that PRR11 expression was up-regulated in glioma tissues, but its role still needs to be further studied. Here, the role of PRR11 in glioma progression and the mechanism were investigated. We found PRR11 was overexpressed in glioma cells. Depletion of PRR11 suppressed the growth of glioma cells as well as induced cell cycle arrest. We further found PRR11 ablation induced the autophagy of glioma cells. Furthermore, knockdown of PRR11 restrained the activation of Akt/mTOR pathway, thereby suppressing the proliferation of glioma cells. We thought PRR11 could serve as a target for glioma therapy.