ArticleInternational journal of biological sciences2023
Inhibition of androgen receptor enhanced the anticancer effects of everolimus through targeting glucose transporter 12.
Article in International journal of biological sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- Integrative bioinformatics analyses identify EDNRA and BCL2L1 as candidate hub genes linking predicted MEHP targets and gastric cancer.Discover oncology · 2026Article
- Targeting the remodeled peritoneal ecosystem: a paradigm shift from tumor cells to the microenvironment in gastric cancer peritoneal metastasis.Frontiers in immunology · 2026Review
- Central Serous Chorioretinopathy Deteriorated With Everolimus Administration in Advanced Renal Cell Carcinoma: A Case Report.Case reports in ophthalmological medicine · 2026Article
- Actionable Genes and Carcinogenic Pathways for Gastric Cancer in Latinos.Cancer medicine · 2025Article
- Evodiamine Boosts AR Expression to Trigger Senescence and Halt Proliferation in OSCC Cells.Current issues in molecular biology · 2025Article
- Identification of Androgen Receptor as a Molecular Docking Target for Survival and Response to Metformin-Induced Ferroptosis in Liver Cancer.Cancer reports (Hoboken, N.J.) · 2025Article
- The glucose transporter GLUT12, a new actor in obesity and cancer.Journal of physiology and biochemistry · 2025Review
- Aging-induced immune microenvironment remodeling fosters melanoma in male mice via γδ17-Neutrophil-CD8 axis.Nature communications · 2024Article
- Advances in active targeting of ligand-directed polymeric nanomicellesRSC advances · 2024Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Everolimus was designed as a mammalian target of rapamycin (mTOR) inhibitor. It has been proven as a targeted drug for gastric cancer (GC) therapy. However, long-term treatment with everolimus may cause severe side effects for recipients. Decreasing the dosage and attenuating the associated risks are feasible to promote clinical translation of everolimus. This study aimed to identify the underlying mechanisms of responses to everolimus and develop novel regimens for GC treatment. Our findings proved that there was a significant dose-dependent relationship of everolimus-induced GC cell apoptosis and glycolysis inhibition. Then, we found that a member of glucose transporter (GLUT12) family, GLUT12, was actively upregulated to counteract the anticancer effects of everolimus. GLUT12 might be overexpressed in GC. High expression of GLUT12 might be correlated with tumor progression and short survival time of GC patients. Bioinformatic analysis suggested that GLUT12 might be involved in regulating cancer development and metabolism. The experiments proved that GLUT12 significantly promoted GC growth, glycolysis and impaired the anticancer effects of everolimus. Androgen receptor (AR) is a classical oncogenic factor in many types of cancer. Everolimus elevated GLUT12 expression in an AR-dependent manner. Inhibition of AR activity abrogated the promotive effects on GLUT12 expression. Both
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