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Published on: August 23, 2019
MicroRNA-340 Mediates Metabolic Shift in Oral Squamous Cell Carcinoma by Targeting Glucose Transporter-1
Ping Xu1, Yan Li2, Haiyuan Zhang2
1Attending Physician, Department of Stomatology, Chengdu Military General Hospital, Chengdu, China.
Purpose:
MicroRNA-340 (miR-340) is deregulated in many human cancers in correlation with tumor progression. Recent studies have found that microRNAs play key roles in energy metabolism. This study explored the contributions of miR-340 to the metabolic shift in oral squamous cell carcinoma (OSCC).
Materials And Methods:
MiR-340 expression was measured by real-time polymerase chain reaction. MiR-340 mimics, miR-340 inhibitor, and scramble small interfering RNA were transfected into SAS human tongue SCC cells to observe their effects on cell proliferation, colony formation, lactate secretion, and glucose uptake rate. Moreover, the relation between the level of miR-340 and glucose transporter-1 (Glut1) was investigated.
Results:
The expression of miR-340 was decreased and thus induced a metabolic switch in oral cancer cells. The decrease in miR-340 increased Glut1 expression, leading to an increase in lactate secretion and glucose uptake rate. The altered metabolism induced by miR-340 resulted in the rapid proliferation of oral cancer cells.
Conclusion:
The findings suggest that miR-340 might act as a molecular switch that contributes to the regulation of glycolysis in OSCC by regulating Glut1 expression.
Insights
MicroRNA-340 (miR-340) downregulation promotes oral cancer growth by increasing glucose metabolism. This metabolic shift, driven by elevated glucose transporter-1 (Glut1), fuels rapid oral squamous cell carcinoma (OSCC) proliferation.
Area of Science:
- Biochemistry
- Molecular Biology
- Oncology
Background:
- MicroRNA-340 (miR-340) is frequently altered in human cancers, impacting tumor progression.
- MicroRNAs are increasingly recognized for their roles in regulating cellular energy metabolism.
- The specific metabolic contributions of miR-340 in oral squamous cell carcinoma (OSCC) remain underexplored.
Purpose of the Study:
- To investigate the role of miR-340 in the metabolic reprogramming of oral squamous cell carcinoma (OSCC).
- To elucidate the relationship between miR-340 expression and key metabolic pathways in OSCC.
Main Methods:
- Quantitative assessment of miR-340 expression using real-time polymerase chain reaction.
- Functional analysis of miR-340 mimics and inhibitors in SAS human tongue SCC cells, evaluating proliferation, colony formation, lactate secretion, and glucose uptake.
- Investigation of the correlation between miR-340 levels and glucose transporter-1 (Glut1) expression.
Main Results:
- Reduced miR-340 expression was observed in oral cancer cells, correlating with a metabolic shift.
- Downregulation of miR-340 led to increased glucose transporter-1 (Glut1) expression.
- Elevated Glut1 expression resulted in heightened lactate secretion and glucose uptake rates, promoting rapid cancer cell proliferation.
Conclusions:
- MiR-340 functions as a critical regulator of glycolysis in OSCC.
- The regulatory mechanism involves modulating glucose transporter-1 (Glut1) expression.
- MiR-340's influence on glycolysis and Glut1 presents a potential therapeutic target for OSCC.
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