ArticleJournal of molecular neuroscience : MN2020
Overexpression of LncRNA PSMG3-AS1 Distinguishes Glioblastomas from Sarcoidosis.
Article in Journal of molecular neuroscience : MN, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Unveiling the oncogenic functions of lncRNA PSMG3-AS1: a review of its biological roles in cancer.Discover oncology · 2025Review
- Innovative perspectives on glioblastoma: the emerging role of long non-coding RNAs.Functional & integrative genomics · 2025Review
- Prognostic and Immune Infiltration Value of Proteasome Assembly Chaperone (PSMG) Family Genes in Lung Adenocarcinoma.International journal of medical sciences · 2023Article
- Long non-coding RNA PSMG3 Antisense RNA 1 is correlated with oral squamous cell carcinoma and regulates cancer cell proliferation by targeting premature microRNA-141.American journal of cancer research · 2023Article
- PSMG3-AS1 enhances glioma resistance to temozolomide via stabilizing c-Myc in the nucleus.Brain and behavior · 2022Article
- Identifying Autophagy-Related lncRNAs and Potential ceRNA Networks in NAFLD.Frontiers in genetics · 2022Article
- Expression of oncogenic long noncoding RNA PSMG3-antisense 1 in lung squamous cell carcinoma.Oncology letters · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In clinical practices, glioblastomas (GBM) in some cases can be misdiagnosed as sarcoidosis. This study aimed to develop a biomarker to distinguish GBM from sarcoidosis. In this study, we found that PSMG3-AS1 was upregulated in plasma of GBM patients in comparison with that in sarcoidosis patients and healthy controls. Receiver operating characteristic (ROC) curve analysis showed that upregulation of PSMG3-AS1 effectively separated GBM patients from sarcoidosis patients and healthy controls. In GBM cells, overexpression of PSMG3-AS1 led to downregulated miR-34a and increased methylation of miR-34a gene. In addition, overexpression of PSMG3-AS1 reduced the inhibitory effects of miR-34a on GBM cell proliferation. In conclusion, overexpression of PSMG3-AS1 distinguishes GBM patients from patients with sarcoidosis, and PSMG3-AS1 may promote GBM cell proliferation by downregulating miR-34a through methylation.
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Registered trials
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