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Fig. 3 | Journal of Experimental & Clinical Cancer Research

Fig. 3

From: Novel role of miR-133a-3p in repressing gastric cancer growth and metastasis via blocking autophagy-mediated glutaminolysis

Fig. 3

Low level of miR-133a-3p is responsible for the induction of autophagy especially in starvation. (a). We used TEM to observe a remarkable accumulation of autophagosomes in the cytoplasm of miR-133a-3p inhibitors transfected GC cells compared with miR-133a-3p mimics transfected cells under starvation. (b). Decreased expression levels of autophagy markers can be observed in miR-133a-3p mimics transfected GC cells. While miR-133a-3p inhibitors transfected cells can be observed an opposite effect. (c). MiR-133a-3p inhibitors transfected cells showed a higher mRFP-GFP-LC3 signal compared with miR-133a-3p mimics and negative control transfected cells, scale bar = 10 μm. (d). Increased trend of EMT was observed in miR-133a-3p IN transfected GC cells while the opposite trend of EMT was observed in miR-133a-3p mimics transfected GC cells compared with NC transfected GC cells by western blot. (e). We observed the increased expression levels of proliferation marker Ki67, EMT marker E-cadherin and autophagy marker LC3 by immunofluorescence in GC organoid models under miR-133a-3p inhibitors treatment compared with negative control, scale bar = 50 μm. All data are presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001

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