Abstract
BackgroundReprogrammed glucose metabolism of enhanced Warburg effect (or aerobic glycolysis) is considered as a hallmark of cancer. Long non-coding RNAs (lncRNAs) have been certified to play a crucial role in tumor progression. The current study aims to inquire into the potential regulatory mechanism of long intergenic non-protein coding RNA 242 (LINC00242) on aerobic glycolysis in gastric cancer.MethodLINC00242, miR-1-3p and G6PD expression levels in gastric cancer tissues and cells were determined by qRT-PCR. Cell apoptosis or viability were examined by Flow cytometry or MTT assay. Western blot was utilized to investigate G6PD protein expression levels. Immunohistochemical (IHC) and hematoxylin and eosin (H&E) staining were used for histopathological detection. The targeted relationship between LINC00242 or G6PD and miR-1-3p was verified by luciferase reporter gene assay. Nude mouse xenograft was utilized to detect tumor formation in vivo.ResultLINC00242 and G6PD was high-expressed in gastric cancer tissues and cells, and LINC00242 is positively correlated with G6PD. Silencing of LINC00242 or G6PD within gastric cancer cells prominently inhibited cell proliferation and aerobic glycolysis in vitro and relieved the tumorigenesis of gastric cancer in vivo. miR-1-3p was predicted to directly target both LINC00242 and G6PD. Overexpression of miR-1-3p suppressed gastric cancer cells proliferation and aerobic glycolysis. LINC00242 competitively combined miR-1-3p, therefore relieving miR-1-3p-mediated suppression on G6PD.ConclusionLINC00242 plays a stimulative role in gastric cancer aerobic glycolysis via regulation of miR-1-3p/ G6PD axis, therefore affecting gastric cancer cell proliferation.
Highlights
Gastric cancer (GC), recognized as stomach adenocarcinoma, is the fifth most frequent malignancies and the third leading cause of cancer-related death worldwide (Smyth et al 2020)
LINC00242 plays a stimulative role in gastric cancer aerobic glycolysis via regulation of miR-1-3p/ Glucose-6-phosphate dehydrogenase (G6PD) axis, affecting gastric cancer cell proliferation
Expression and prognosis significance of G6PD in gastric cancer Based on microarray analyses, we respectively filtered out 18 highly expressed mRNAs and 4 lowly expressed mRNAs in the gastric cancer tissue samples based on Gene Expression Omnibus (GEO) microarray and visualized them in heat-maps (Fig. 1a)
Summary
Gastric cancer (GC), recognized as stomach adenocarcinoma, is the fifth most frequent malignancies and the third leading cause of cancer-related death worldwide (Smyth et al 2020). Warburg effect (or aerobic glycolysis), a characteristic tumor cell phenotype, can expedite tumor progression by accelerating lactate production and glucose uptake (Liberti and Locasale 2016). The augment in activity and/or expression of some crucial glycolytic enzymes, such as lactate dehydrogenase A (LDHA)(Jin et al 2017), hexokinase 2 (HK2) (Garcia et al 2019) and glucose transporter isoform 1 (GLUT1) (Zambrano et al 2019) had been discovered in a large amount of human tumors. Glucose-6-phosphate dehydrogenase (G6PD) is discovered in almost all cells, and is the rate-limiting step of the pentose phosphate pathway (PPP) (Stanton 2012). The current study aims to inquire into the potential regulatory mechanism of long intergenic non-protein coding RNA 242 (LINC00242) on aerobic glycolysis in gastric cancer
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