Targeting Long Noncoding RNA HMMR-AS1 Suppresses and Radiosensitizes Glioblastoma

Abstract

Emergent evidences revealed that long noncoding RNAs (lncRNAs) participate in neoplastic progression. HMMR is an oncogene that is highly expressed in glioblastoma (GBM) and supports GBM growth. Whether lncRNAs regulate HMMR in GBM remains unknown. Herein, we identify that an HMMR antisense lncRNA, HMMR-AS1, is hyperexpressed in GBM cell lines and stabilizes HMMR mRNA. Knockdown of HMMR-AS1 reduces HMMR expression; inhibits cell migration, invasion, and mesenchymal phenotypes; and suppresses GBM cell growth both in vitro and in vivo. Moreover, knockdown of HMMR-AS1 radiosensitizes GBM by reducing DNA repair proteins ATM, RAD51, and BMI1. Our data demonstrate a mechanism of sense-antisense interference between HMMR and HMMR-AS1 in GBM and suggest that targeting HMMR-AS1 is a potential strategy for GBM treatment.