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Updated: Feb 7, 2026

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
Published on: April 7, 2017
Blocking LINC00152 suppresses glioblastoma malignancy by impairing mesenchymal phenotype through the
Jinquan Cai1,2, Jinwei Zhang1,2, Pengfei Wu1,2
1Department of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, No.246, Xuefu Road, Nangang District, Harbin, 150086, China.
Introduction:
Glioblastoma, the most common and mortal primary brain tumor, accompanied with a dismal clinical outcome in adults. The oncogenic functions of long non-coding RNAs (lncRNAs) in glioblastoma have not been completely illuminated. In the present study, we aimed to investigate the potential role of lncRNA LINC00152 in glioblastoma.
Methods:
We used bioinformatic method in public databases to select lncRNA LINC00152 and investigate its clinical value and potential mechanism in glioblastoma. CCK-8, transwell assay, colony formation and wound healing assays were used to explore the role of LINC00152 in glioblastoma malignant behaviors. PCR, western blot, immunofluorescence, reporter assays and nude mouse tumor intracranial model were employed to further verify the regulatory mechanism of LINC00152 in glioblastoma.
Results:
LINC00152 was closely associated with glioma WHO classification and poor prognosis, and indicated a poor prognosis in glioblastoma patients. Tumor growth and invasion were suppressed both in vitro and vivo after LINC00152 was blocked. Moreover, LINC00152 modulated GBM malignant progression and proneural-mesenchymal transition through the miR-612 dependent AKT2/NF-κB pathway.
Conclusions:
LINC00152 acted as a tumor oncogene with prognostic value for patients with glioblastoma through LINC00152/miR-612/AKT2/NF-κB axis.
Insights
Long non-coding RNA LINC00152 promotes glioblastoma growth and invasion. Blocking LINC00152 suppresses tumor progression via the miR-612/AKT2/NF-κB pathway, indicating its prognostic value.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Glioblastoma is a deadly primary brain tumor with poor outcomes.
- The role of long non-coding RNAs (lncRNAs) in glioblastoma oncogenesis requires further elucidation.
Purpose of the Study:
- To investigate the role of lncRNA LINC00152 in glioblastoma.
- To explore its clinical significance and underlying molecular mechanisms.
Main Methods:
- Bioinformatic analysis of public databases to identify LINC00152.
- In vitro assays (CCK-8, transwell, colony formation, wound healing) to assess malignant behaviors.
- In vivo studies using a nude mouse intracranial model and molecular techniques (PCR, Western blot, immunofluorescence, reporter assays) to verify mechanisms.
Main Results:
- LINC00152 expression correlates with glioma WHO classification and predicts poor glioblastoma prognosis.
- Inhibition of LINC00152 suppressed glioblastoma growth and invasion both in vitro and in vivo.
- LINC00152 promotes glioblastoma progression and epithelial-mesenchymal transition via the miR-612-dependent AKT2/NF-κB pathway.
Conclusions:
- LINC00152 functions as an oncogene in glioblastoma.
- LINC00152 holds prognostic value for glioblastoma patients.
- The LINC00152/miR-612/AKT2/NF-κB axis is crucial for glioblastoma pathogenesis.
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