Related Experiment Video
Updated: Nov 16, 2025
Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
Published on: July 21, 2018
PolG Inhibits Gastric Cancer Glycolysis and Viability by Suppressing PKM2 Phosphorylation
Mengzhu Lv1, Simeng Zhang2, Yuqing Dong1
1Department of Plastic Surgery, China Medical University the First Hospital, Shenyang, 110001, Liaoning Province, People's Republic of China.
Purpose:
Gastric cancer (GC) is the fifth most frequently diagnosed cancer and the third leading cause of cancer-related death. There is a critical need for the development of novel therapies in GC. DNA polymerase gamma (PolG) has been implicated in mitochondrial homeostasis and affects the development of numerous types of cancer, however, its effects on GC and molecular mechanisms remain to be fully determined. The aim of the present research was to clarify the effects of PolG on GC and its possible molecular mechanism of action.
Methods:
The GSE62254 dataset was used to predict the effect of PolG on prognostic value in GC patients. Lentivirus-mediated transduction was used to silence PolG expression. Western blot analysis evinced the silencing effect. Co-immunoprecipitation (Co-IP) analysis was performed to explore the potential molecular mechanism of action. Analysis of the glycolysis process in GC cells was also undertaken. Cell proliferation was determined using a CCK-8 (Cell Counting Kit-8) proliferation assay. Cell migration was detected using the Transwell device. Animal experiments were used to measure in vivo xenograft tumor growth.
Results:
GC patients with low PolG expression have worse overall survival (OS) and progression-free survival (PFS). PolG binds to PKM2 and affects the activation of Tyr105-site phosphorylation, thus interfering with the glycolysis of GC cells. In vitro tumor formation experiments in mice also confirmed that PolG silencing of GC has a stronger proliferation ability. PolG can suppress GC cell growth both in vivo and in vitro.
Conclusion:
Our study reveals a potential molecular mechanism between PolG and the energy metabolic process of GC tumor cells for the first time, suggesting PolG as an independent novel potential therapeutic target for tumor therapy, and providing new ideas for clinical GC treatment.
Insights
DNA polymerase gamma (PolG) suppresses gastric cancer (GC) growth by interfering with glycolysis. Low PolG expression correlates with poor survival, indicating PolG as a potential therapeutic target for GC.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Metabolism
Background:
- Gastric cancer (GC) is a leading cause of cancer death, necessitating novel therapeutic strategies.
- DNA polymerase gamma (PolG) plays a role in mitochondrial homeostasis and various cancers, but its specific function in GC is unclear.
- Understanding PolG's mechanism in GC is crucial for developing targeted treatments.
Purpose of the Study:
- To investigate the role of DNA polymerase gamma (PolG) in gastric cancer (GC) progression.
- To elucidate the molecular mechanisms underlying PolG's effects on GC.
- To assess PolG's potential as a therapeutic target for GC.
Main Methods:
- Utilized the GSE62254 dataset to analyze PolG's prognostic value in GC patients.
- Employed lentivirus-mediated transduction to silence PolG expression and confirmed via Western blot.
- Investigated PolG's interaction with PKM2 using co-immunoprecipitation (Co-IP) and assessed glycolysis, proliferation, and migration.
- Evaluated tumor growth in vivo using animal models.
Main Results:
- Lower PolG expression in GC patients correlated with reduced overall survival (OS) and progression-free survival (PFS).
- PolG interacts with PKM2, inhibiting Tyr105 phosphorylation and consequently affecting GC cell glycolysis.
- Silencing PolG enhanced GC cell proliferation in vitro and tumor growth in vivo, indicating PolG suppresses GC progression.
Conclusions:
- This study identifies a novel molecular mechanism linking PolG to the energy metabolism of GC cells.
- PolG acts as a suppressor of GC cell growth both in vitro and in vivo.
- PolG emerges as a promising independent therapeutic target for gastric cancer treatment.
More Related Videos
11:13Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment
Published on: June 9, 2023
09:18Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
Published on: December 27, 2016
Related Concept Videos
02:23Abnormal Proliferation
02:34Inhibition of Cdk Activity
03:03mTOR Signaling and Cancer Progression
The mTOR pathway or the...
01:22PI3K/mTOR/AKT Signaling Pathway
01:19Interactions Between Signaling Pathways
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
02:53Adaptive Mechanisms in Cancer Cells
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...