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MiR-195-5p Reduces Esophageal Cancer Cell Proliferation Through The IGF-1R/AKT Axis
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Abstract
Background
Esophageal cancer (ECa) remains a major cause of mortality across the globe. The expression of MiR-195-5p is altered in a plethora of tumors, but its role in ECa development and progression are undefined.
Result
Here, we show that miR-195-5p is downregulated in ECa and associated with poor survival in ECa. Function assays indicated that MiR-195-5p inhibited ECa progression. Mechanistically, we identified IGF-1R as a downstream target of miR-195-5p, and miR-195-5p/IGFR axis caused a loss of GLUT1 expression, reduced glucose uptake, reduced lactate production, and low levels of ATP production.
Conclusion
Collectively, miR-195-5p as a Eca suppressor impaired glycolysis. This highlighting miR-195-5p as a novel target for much needed anti-ECa therapeutics.
Title: MiR-195-5p Reduces Esophageal Cancer Cell Proliferation Through The IGF-1R/AKT Axis
Description:
Abstract
Background
Esophageal cancer (ECa) remains a major cause of mortality across the globe.
The expression of MiR-195-5p is altered in a plethora of tumors, but its role in ECa development and progression are undefined.
Result
Here, we show that miR-195-5p is downregulated in ECa and associated with poor survival in ECa.
Function assays indicated that MiR-195-5p inhibited ECa progression.
Mechanistically, we identified IGF-1R as a downstream target of miR-195-5p, and miR-195-5p/IGFR axis caused a loss of GLUT1 expression, reduced glucose uptake, reduced lactate production, and low levels of ATP production.
Conclusion
Collectively, miR-195-5p as a Eca suppressor impaired glycolysis.
This highlighting miR-195-5p as a novel target for much needed anti-ECa therapeutics.
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