Abstract
ObjectiveGlutamate ionotropic receptor N-methyl-d-aspartate (NMDA) type subunit 2D (GRIN2D) is a member of the GRIN gene family and contributes to the development and function of the brain. GRIN2D was found to be upregulated in several types of cancers; however, its mechanism in lung adenocarcinoma (LUAD) remains unclear. MethodsWe determined the role of GRIN2D in LUAD. In addition, we investigated the potential mechanism of GRIN2D in LUAD using bioinformatics analysis and confirmed this mechanism using biological approaches. ResultsGRIN2D was found to be upregulated in LUAD tissues and cells. GRIN2D knockdown reduced the proliferation and accelerated the apoptosis of LUAD cells. GRIN2D also activated glycolysis, gluconeogenesis, and the E2F signalling pathway in LUAD. GRIN2D knockdown significantly inhibited glucose uptake, lactate production, the ATP/ADP ratio, ECAR, and OCR in LUAD cells. E2F1 overexpression eliminated the inhibitory effect of GRIN2D knockdown in LUAD cells. ConclusionsGRIN2D knockdown suppresses cell growth, migration, glycolysis, and gluconeogenesis of LUAD by inhibiting the E2F signalling pathway.
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