ArticleCellular and molecular neurobiology2021
LncRNA SAMMSON Knockdown Inhibits the Malignancy of Glioblastoma Cells by Inactivation of the PI3K/Akt Pathway.
Article in Cellular and molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Long non-coding RNAs in glioblastoma: from molecular drivers to therapeutic targets.Frontiers in immunology · 2026Review
- Innovative perspectives on glioblastoma: the emerging role of long non-coding RNAs.Functional & integrative genomics · 2025Review
- Long Non-Coding RNAs in Malignant Human Brain Tumors: Driving Forces Behind Progression and Therapy.International journal of molecular sciences · 2025Review
- Functional Bidirectionality of ERV-Derived Long Non-Coding RNAs in Humans.International journal of molecular sciences · 2024Review
- lncRNA Biomarkers of Glioblastoma Multiforme.Biomedicines · 2024Review
- The oncogenic role of SAMMSON lncRNA in tumorigenesis: A comprehensive review with especial focus on melanoma.Journal of cellular and molecular medicine · 2023Review
- Bioinformatic Identification of Potential RNA Alterations on the Atrial Fibrillation Remodeling from Human Pulmonary Veins.International journal of molecular sciences · 2023Article
- Article
- lncHUB2: aggregated and inferred knowledge about human and mouse lncRNAs.Database : the journal of biological databases and curation · 2023Article
- Long Noncoding RNA SAMMSON Promotes Melanoma Progression by Inhibiting FOXA2 Expression.Stem cells international · 2023Article
- An Unanticipated Modulation of Cyclin-Dependent Kinase Inhibitors: The Role of Long Non-Coding RNAs.Cells · 2022Review
- Comprehensive analysis of cuproptosis-related long non-coding RNA signature and personalized therapeutic strategy of breast cancer patients.Frontiers in oncology · 2022Article
- Article
- LncRNA SAMMSON Overexpression Suppresses Vascular Smooth Muscle Cell Proliferation via Inhibiting miR-130a Maturation to Participate in Intracranial Aneurysm.Neuropsychiatric disease and treatment · 2021Article
- Long Non-Coding RNA UBA6-AS1 Promotes the Malignant Properties of Glioblastoma by Competitively Binding to microRNA-760 and Enhancing Homeobox A2 Expression.Cancer management and research · 2021Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysregulated lncRNAs are proposed to be tightly associated with the progression of various tumors including glioblastoma (GBM). LncRNA Survival Associated Mitochondrial Melanoma-Specific Oncogenic Non-Coding RNA (SAMMSON) has been reported to be an oncogenic lncRNA in several tumors. Nevertheless, the specific role and molecular mechanism of SAMMSON in GBM progression remain unknown. Expression of SAMMSON in GBM tissues and cells was detected by qRT-PCR. CCK-8 and LDH release assays were applied to evaluate cellular viability. Invasion effect was assessed by Transwell invasion assay and western blot analysis of E-cadherin and N-cadherin expression. Apoptosis was detected using flow cytometry analysis and caspase-3 activity assay. The protein levels of phosphatidylinositol-3-kinase (PI3K), phosphorylated (p)-PI3K, protein kinase B (Akt) and p-Akt were estimated by western blot. We found that SAMMSON was highly expressed in GBM tissues and cells. SAMMSON knockdown suppressed cell viability and increased LDH release in GBM cells. Moreover, SAMMSON silencing impeded the invasive ability of GBM cells by regulating epithelial-to-mesenchymal transition (EMT). Furthermore, SAMMSON downregulation increased the apoptotic rate and caspase-3 activity in GBM cells. Additionally, it was demonstrated that the PI3K/Akt pathway was inhibited following SAMMSON silencing in GBM cells. Rescue assays revealed that activation of the PI3K/Akt pathway by 740Y-P abolished SAMMSON knockdown-induced viability reduction, invasion suppression and apoptosis in GBM cells. Taken together, lncRNA SAMMSON knockdown inhibited the malignancy of GBM cells by inactivation of the PI3K/Akt pathway.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.