ArticleNeurochemical research2025
Regulation of Glycolysis by SMAD5 in Glioma Cells: Implications for Tumor Growth and Apoptosis.
Article in Neurochemical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Novel approaches to modulate CAR-T cell function by targeting the tumor microenvironment in ovarian cancer.Journal of ovarian research · 2026Review
- Hydroxytyrosol and Brain Tumors: Mechanisms of Action and Therapeutic Potential.Current issues in molecular biology · 2025Review
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Authors and funding
7 authors.
Funding
Abstract
The Warburg effect serves as a crucial aspect of tumor metabolism, where tumor cells preferentially rely on glycolysis, despite its lower efficiency, over oxidative phosphorylation for energy production even under aerobic conditions. This reprogramming of glucose metabolism confers glioma cells with the capacity for survival and proliferation. Serving as a messenger for regulating transforming growth factor beta, intracellular pH, cell metabolism maintaining cellular bioenergetic homeostasis, SMAD family member 5 (SMAD5) plays a pivotal role in the malignant progression of glioma cells and aerobic glycolysis. Hence, we have identified the expression and function of SMAD5 in human glioma cells, aiming to clarify its role in glycolysis. qRT-PCR and Western blot, reveal that SMAD5 is significantly overexpressed in glioma cells. Knocking down SMAD5 can effectively suppress the proliferation and invasion of glioma cells, while promoting apoptosis, furthermore, downregulation of SMAD5 in vivo has been shown to significantly reduce the growth of xenograft tumors. Conversely, overexpressing SMAD5 enhances the proliferative and invasive capabilities of glioma cells, while suppressing apoptosis. Concurrently, alterations in the expression level of SMAD5 exert an impact on the expression of glucose transporter GLUT1 and crucial enzymes involved in glycolysis, namely HK2 and PKM2, ultimately influencing the glycolytic capability of glioma cells. Specifically, knockdown of SMAD5 suppresses glycolysis, whereas its overexpression enhances glycolytic activity. In conclusion, our data demonstrate that SMAD5 can influence the proliferation, invasion, and apoptosis of glioma cells by modulating glycolysis. This finding holds potential for the development of novel metabolic treatment strategies for glioma.
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Registered trials
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