ArticleCancer biology & medicine2021
BYSL contributes to tumor growth by cooperating with the mTORC2 complex in gliomas.
Article in Cancer biology & medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 34 citations in OpenAlex.
- Immune pathway activation in gastric cancers with LINE-1 retrotransposon overexpression and homologous recombination deficiency.Experimental & molecular medicine · 2026Article
- Investigation of the expression and potential mechanistic role of BYSL in acute myeloid leukemia.Clinical and experimental medicine · 2026Article
- The atypical kinase right open reading frame kinase 1 suppresses glioma cell growth through mammalian target of rapamycin inhibition and apoptotic signaling activation.Translational cancer research · 2026Article
- Tissue-Specific Multi-Omics Integration Demonstrates Molecular Signatures Connecting Obesity to Immune Vulnerability.Metabolites · 2026Article
- The WW domain presents a promising target for the development of PCIF1 agonists in the treatment of glioma.NPJ precision oncology · 2025Article
- Proteomics and lipidomics of human umbilical cord mesenchymal stem cells exposed to ionizing radiation.European journal of medical research · 2025Article
- Bystin is a Prognosis and Immune Biomarker: From Pan-Cancer Analysis to Validation in Breast Cancer.Breast cancer (Dove Medical Press) · 2025Article
- ITGA1 Promotes Glioma Cell Proliferation and Affects Immune Cell Infiltration in Low-Grade Glioma.Mediators of inflammation · 2024Article
- Identification of ZMYND19 as a novel biomarker of colorectal cancer: RNA-sequencing and machine learning analysis.Journal of cell communication and signaling · 2023Article
- Using integrated analysis from multicentre studies to identify RNA methylation-related lncRNA risk stratification systems for glioma.Cancer cell international · 2023Article
- Integrative proteogenomic characterization of hepatocellular carcinoma across etiologies and stages.Nature communications · 2022Review
- Increased expression of NOP14 is associated with improved prognosis due to immune regulation in colorectal cancer.BMC gastroenterology · 2022Article
- Pan-cancer analyses reveal multi-omics and clinical characteristics of RIO kinase 2 in cancer.Frontiers in chemistry · 2022Article
- Methionine deprivation inhibits glioma growth through downregulation of CTSL.American journal of cancer research · 2022Article
- The Mechanism Study of Common Flavonoids on Antiglioma Based on Network Pharmacology and Molecular Docking.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- New Selective Inhibitors of ERG Positive Prostate Cancer: ERGi-USU-6 Salt Derivatives.ACS medicinal chemistry letters · 2021Article
- Hypoxia-Induced miR-378a-3p Inhibits Osteosarcoma Invasion and Epithelial-to-Mesenchymal TransitionFrontiers in genetics · 2021Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Methods: BYSL expression in glioma tissues was measured by quantitative real-time PCR, Western blot, and immunohistochemistry. Results: The BYSL mRNA and protein levels were elevated in glioma tissues. Silencing BYSL inhibited glioma cell proliferation, impeded cell cycle progression, and induced apoptosis, whereas overexpressing BYSL protein led to the opposite effects. We identified a complex consisting of BYSL, RIOK2, and mTOR, and observed co-localization and positive correlations between BYSL and RIOK2 in glioma cells and tissues. Overexpressing BYSL or RIOK2 increased the expression and activity of AKT/mTOR signaling molecules, whereas downregulation of BYSL or RIOK2 decreased the activity of AKT/mTOR signaling molecules. Silencing BYSL or RIOK2 decreased the growth of the tumors and prolonged the lifespan of the animals in an orthotopic xenograft model. Conclusions: High expression of BYSL in gliomas promoted tumor cell growth and survival both
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