Related Experiment Video
Updated: Feb 10, 2026
Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
Published on: August 23, 2024
TNKS1 mediates the PTEN-PI3K/AKT pathway to regulate glycolysis and proliferation in gliomas
Zhenyan Shi1, Danke Shen1, Jie Wu1
1Department of Neurosurgery, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, China.
Objective:
To explore the mechanisms by which TNKS1 regulates glycolysis and proliferation in glioma.
Methods:
Cell viability was assessed using the CCK-8 assay. Levels of glucose and lactate were measured using biochemical detection kits. Western blotting was used to detect the expression levels of glycolysis-related proteins, and qPCR was employed to measure the mRNA expression of GLUT1 and HK2. A subcutaneous xenograft tumor model in nude mice was established. After intratumoral injection of drugs, the effects of TNKS1 knockdown on tumor tissues were observed using HE staining and immunohistochemical staining. Western blotting was also used to detect the expression of PTEN and other proteins in glioma tissues.
Results:
Compared with the control group, TNKS1 knockdown resulted in increased expression of PTEN, decreased expression of PI3K and p-AKT/AKT proteins, reduced cell proliferation capacity, and lower glucose uptake and lactate production. The results were opposite in the TNKS1 overexpression group. In the group treated with a PI3K agonist compared with the untreated group, the expression of PI3K and p-AKT/AKT proteins increased, and cell proliferation capacity, glucose uptake, and lactate production also increased to varying degrees. In the TNKS1 overexpression + PI3K inhibitor group compared with the TNKS1 overexpression group, the expression of PI3K and p-AKT/AKT proteins decreased, and cell proliferation capacity, glucose uptake, and lactate production also decreased to varying degrees. In the in vivo experiments, compared with the control group, the TNKS1 knockdown group showed increased tumor cell apoptosis and necrosis. Immunohistochemical and Western blotting analyses indicated that compared with the TNKS1-siRNA empty vector group, the TNKS1-siRNA group had significantly increased PTEN protein expression. The expression levels of PI3K, p-AKT/AKT proteins, and Ki67 were significantly lower in the TNKS1-siRNA group, inhibitor group, and TNKS1-siRNA + inhibitor group.
Conclusion:
TNKS1 regulates glycolysis and proliferation in glioma by mediating the PTEN-PI3K/AKT pathway.
Insights
Tankyrase 1 (TNKS1) regulates glioma cell growth and energy metabolism by influencing the PTEN-PI3K/AKT pathway. TNKS1 knockdown inhibits tumor progression and glycolysis in glioma.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Glioma is a primary brain tumor with complex regulatory mechanisms.
- Glycolysis and cell proliferation are critical processes in tumor development.
- Understanding the molecular drivers of glioma is essential for targeted therapies.
Purpose of the Study:
- To elucidate the role of Tankyrase 1 (TNKS1) in regulating glycolysis and proliferation in glioma.
- To investigate the underlying molecular pathways, specifically the PTEN-PI3K/AKT signaling cascade.
Main Methods:
- Cell viability assays (CCK-8), glucose/lactate measurements, Western blotting, and qPCR were used.
- A subcutaneous xenograft nude mouse model was employed for in vivo validation.
- Immunohistochemical staining assessed tumor tissue changes.
Main Results:
- TNKS1 knockdown decreased cell proliferation, glucose uptake, and lactate production, while increasing PTEN expression and decreasing PI3K/p-AKT/AKT levels.
- TNKS1 overexpression showed opposite effects.
- In vivo studies confirmed reduced tumor growth, increased apoptosis, and necrosis upon TNKS1 knockdown.
Conclusions:
- TNKS1 plays a significant role in promoting glioma glycolysis and proliferation.
- The PTEN-PI3K/AKT pathway is a key mediator of TNKS1's effects in glioma.
- Targeting TNKS1 may offer a therapeutic strategy for glioma treatment.
Related Concept Videos
01:22PI3K/mTOR/AKT Signaling Pathway
00:56What is Glycolysis?
Cells make energy by breaking down macromolecules. Cellular respiration is the biochemical process that converts "food energy" (from the chemical bonds of macromolecules) into chemical energy in the form of adenosine triphosphate (ATP). The first step of this tightly regulated and intricate process is glycolysis. The word glycolysis originates from the Latin glyco (sugar) and lysis (breakdown). Glycolysis serves two main intracellular functions: generating ATP and generating...
01:13Outcomes of Glycolysis
Cellular respiration can occur aerobically (with oxygen) or anaerobically (without oxygen). In the presence of oxygen, cellular respiration starts with glycolysis and continues with pyruvate...
01:28Energy-releasing Steps of Glycolysis
The first energy-releasing step—the 6th step of glycolysis...
01:20Energy-requiring Steps of Glycolysis
01:23Glycolysis