Targeting long non-coding RNA PVT1/TGF-β/Smad by p53 prevents glioma progression

Glioma is a primary intracranial malignant tumor with poor prognosis, and its pathogenesis is unclear. This study discussed the impact of p53/IncRNA plasmacytoma variant translocation 1 (IncRNA PVT1)/transforming growth factor beta (TGF-beta)/Smad axis on the biological characteristics of glioma. Glioma and normal tissues were collected, in which relative IncRNA PVT1 and p53 expression was assessed. Pearson's analysis was adopted for the correlation analysis between IncRNA PVT1 and p53. Short interfering RNA (siRNA) against IncRNA PVT1 (siRNA-PVT1), siRNA-p53 or both was transfected into the glioma cells to evaluate effects of IncRNA PVT1 and p53 on cell proliferation, migration, invasion, and apoptosis. Mouse xenograft model of glioma was established to verify function of IncRNA PVT1 and p53 in vivo. Relationship among p53, IncRNA PVT1 and TGF-13/Smad was predicted and confirmed. Glioma tissues and cells showed downregulated p53 expression and increased IncRNA PVT1 expression. An adverse relationship was noted between p53 expression and IncRNA PVT1 expression. p53 was shown to be enriched in the IncRNA PVT1 promoter region and resulted in its suppression. p53 inhibited glioma cell proliferation, migration, and invasion, and induced apoptosis as well as arrested tumor growth by downregulating IncRNA PVT1. LncRNA PVT1 was found to bind to TGF-beta and activate TGF-beta/Smad pathway, promoting progression of glioma. Consequently, p53 exerts anti-oncogenic function on glioma development by suppressing IncRNA PVT1 and subsequently inactivating TGF-beta/Smad pathway.

Automated summary

This study discovered that p53 exerts anti-oncogenic function on glioma development by suppressing IncRNA PVT1 and subsequently inactivating TGF-beta/Smad pathway.