Competitive Sequestration of miR-1183 by lncRNA DDX11-AS1 Drives Gliomagenesis through E2F7 Activation.

Objectives: Glioma, as the most lethal primary brain malignancy with poor prognosis, requires further elucidation on the functional role of long noncoding RNA (lncRNA) DDX11 antisense RNA 1 (DDX11-AS1) in its pathogenesis, despite its established oncogenic functions in other cancers. Therefore, this study sought to characterize the oncogenic role and molecular mechanism of DDX11-AS1 in glioma. Methods: DDX11-AS1 expression levels were analyzed in clinical surgical glioma specimens and publicly available datasets. The functional roles of DDX11-AS1 on glioma cell proliferation and migration were investigated using in vitro knockdown and overexpression assays. In vivo tumor growth was assessed using orthotopic glioma-bearing mouse models. To elucidate the regulatory axis involving DDX11-AS1, miR-1183, and E2F transcription factor 7 (E2F7), we performed competitive endogenous RNA (ceRNA) analysis and conducted functional rescue experiments via miR-1183 inhibition. Results: DDX11-AS1 expression was markedly upregulated in clinical glioma specimens. Functionally, DDX11-AS1 knockdown significantly suppressed glioma cell proliferation and migration in vitro, while its overexpression exacerbated these malignant phenotypes. Orthotopic glioma-bearing mouse models confirmed that DDX11-AS1 drives in vivo glioma tumor growth. Mechanistically, DDX11-AS1 functions as a ceRNA by competitively interacting with miR-1183. Critically, inhibition of miR-1183 rescued the suppressive effects of DDX11-AS1 knockdown on glioma tumorigenic phenotypes and restored E2F7 expression levels. Conclusions: This study demonstrates that lncRNA DDX11-AS1 promotes glioma progression by regulating the miR-1183/E2F7 axis, indicating a potential therapeutic target for glioma.