miR-1289 promotes glioblastoma tumorigenesis via targeting EFNA5.

Authors

Yunyun Li, Lu Wang

Published in

Brain research. Pages 150526. Sep 03, 2026. Epub Sep 03, 2026.

Abstract

miR-1289 is dysregulated in various cancers, but its mechanism in glioblastoma (GBM) remains unclear.
This study sought to examine the association between miR-1289 expression and GBM patients' clinical prognosis, and its effect on GBM cell biological behaviors.
qRT-PCR was used to measure miR-1289 and EFNA5 expression. Kaplan-Meier (KM) survival analysis was used to assess the association of miR-1289 expression and patient survival probability, and a multivariate Cox regression model was utilized to assess its prognostic value. CCK-8 and Transwell assays were utilized to detect GBM cell migration, invasion, and proliferation. Potential target genes of miR-1289 were computationally predicted via an integrated approach using the miRDB database. The direct binding between miR-1289 and EFNA5 was experimentally validated via dual-luciferase reporter assays.
miR-1289 was highly expressed in GBM. High miR-1289 expression in GBM correlated with notably shorter survival, and it served as a GBM prognostic marker. Downregulation of miR-1289 significantly inhibited GBM cells' malignant behaviors. Mechanistically, miR-1289 could directly target and regulate EFNA5, and their expressions were negatively correlated in GBM. Knockdown of EFNA5 reversed the tumor-suppressive effect induced by miR-1289 downregulation.
miR-1289 has the potential to be a prognostic biomarker for GBM and promotes the malignant biological behaviors of GBM cells by targeting EFNA5.

PMID:
42692382
Bibliographic data and abstract were imported from PubMed on 04 Sep 2026.

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