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Fig. 5 | Molecular Cancer

Fig. 5

From: The lncRNA MACC1-AS1 promotes gastric cancer cell metabolic plasticity via AMPK/Lin28 mediated mRNA stability of MACC1

Fig. 5

MACC1-AS1 promotes metabolic plasticity in GC cells though MACC1 regulation. a qPCR results showing that MACC1-AS1 was located in cytoplasm by fractionation and detection of nuclear and cytoplasmic MACC1-AS1. b-c qPCR and western blottingresults showing that MACC1-AS1 promoted MACC1 expression at the mRNA and protein level; **P < 0.01. d Combined IF/FISH results showing that MACC-AS1 promoted MACC1 expression, while had no influence on the cytoplasm-nuclear distribution of MACC1. e Western blotting results showing that MACC1-AS1 did not affect the distribution of MACC1 in the cytoplasm and nucleus. f Luciferase assays indicating that MACC1-AS1 did not influence MACC1 promoter transcriptional activity in MKN45 either in conditions of normal or deprived glucose. g MACC1-AS1 did not affect protein stability, as assessed by cyclohexamide-induced MACC1 degradation (100 μg/mL), and subsequent western blotting. h Decreased MACC1 expression by shRNA interference was reversed by MACC1-AS1 overexpression, based on western blotting. i MACC1-AS1 partially reversed the MACC1 shRNA-induced GLUT1, HK2, and LDH suppression based on western blotting. j Western blotting results showing that MACC1-AS1 maintained GLUT1 and HK2 expression under glucose deprivation. k-l NADPH and GSH were decreased after MACC1 silencing, while this effect was abrogated by MACC1-AS1 overexpression

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