ArticleCell biology and toxicology2022
LINC02308 promotes the progression of glioma through activating mTOR/AKT-signaling pathway by targeting miR-30e-3p/TM4SF1 axis.
Article in Cell biology and toxicology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 13 citations in OpenAlex.
- A new ferroptosis-related signature model including messenger RNAs and long non-coding RNAs predicts the prognosis of gastric cancer patients.Journal of translational internal medicine · 2023Article
- Identifying tumour microenvironment-related signature that correlates with prognosis and immunotherapy response in breast cancer.Scientific data · 2023Article
- PSMG3-AS1 enhances glioma resistance to temozolomide via stabilizing c-Myc in the nucleus.Brain and behavior · 2022Article
- Clues for Improving the Pathophysiology Knowledge for Endometriosis Using Plasma Micro-RNA Expression.Diagnostics (Basel, Switzerland) · 2022Article
- Potential diagnostic of lymph node metastasis and prognostic values of TM4SFs in papillary thyroid carcinoma patients.Frontiers in cell and developmental biology · 2022Article
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Authors and funding
4 authors at 2 institutions in 1 country.
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Abstract
backgroundGlioma is a common brain malignancy, and the purpose of this study is to investigate the function of LINC02308 in glioma.
methodsThe differentially expressed lncRNAs were screened by microarray. The expression of LINC02308 in glioma tissues and cells was evaluated. The interaction among LINC02308, miR-30e-3p, and TM4SF1 was determined. Cell proliferation and apoptosis were evaluated. The expression of mTOR/AKT-signaling and apoptosis-related markers was detected by Western blot. A xenograft tumor mouse model was constructed to investigate the roles of LINC02308.
resultsLINC02308 was significantly overexpressed in glioma, and a high LINC02308 level was correlated with a poor prognosis. LINC02308 silencing markedly inhibited proliferation and reduced apoptosis of glioma cells and also suppressed tumor growth in the xenograft tumor mouse model. Finally, we demonstrated that LINC02308 played its oncogenic role through binding to miR-30e-3p so as to relieve miR-30e-3p-induced suppression of TM4SF1.
conclusionsLINC02308 promoted glioma tumorigenesis as a sponge of miR-30e-3p to upregulate TM4SF1 and activate AKT/mTOR pathway. Graphical Abstract Hypothesis diagram illustrates the function and mechanism of LINC02308 in glioma. A schematic representation of the functional mechanism of LINC02308 in glioma.
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