Fig 1: EWS cells uptake extracellular glutamine via the glutamine transporter SLC1A5. (A) Exon level expression and fold-change from RNA-seq analysis (Log2 TPM) of the expression of SLC1A4 and SLC1A5 in control (siNeg) and EWS-FLI1-silenced TC32 cells (siEWSR1 or siFLI1). (B) Violin scatter plots (including median and quartiles) of the expression of SLC1A4 and SLC1A5 in EWS-FLI1 positive EWS primary tumors (n = 58), EWS-FLI1 positive EWS cell lines (n = 33) and normal tissues (n = 42). (C) qPCR analysis of the expression of the indicated genes (relative to siNeg-transfected cells, mean ± s.e.m., n = 3) in EWS-FLI1-silenced TC32 cells (48 h). (D) Fold-enrichment of EWS-FLI1-co-precipitating DNA determined by qPCR of genomic DNA spanning putative EWS-FLI1 binding sites. Data shown were calculated as a percent of input DNA and the fold-enrichment of the anti-FLI1 antibody compared to IgG; triplicate samples of each treatment in each experiment. (E) Glycine levels in siRNA or compound-treated TC32 and SKNMC cells (mean ± SEM of three independent experiments). (B) Unpaired adjusted t-test ***P < 0.001 n.s. = non-significant.; (C and E) Two-way ANOVA (adjusted P-value) ***P < 0.001; (D) Unpaired t-test, corrected for multiple comparisons ***P < 0.001
Fig 2: SREBF2 is highly associated with GLS or SLC1A5 in human HCC specimens.(A) Representative IHC images and statistical data of SREBF2, GLS and SLC1A5 in human HCC versus adjacent normal liver tissues were displayed, respectively. Data present as mean ± SD. ***p < 0.001.(B) Kaplan-Meier curves showed the survival of individuals with HCC from TCGA database, separating based on the expression of SREBF2, GLS and SLC1A5.(C) The correlation of SREBF2 with GLS or SLC1A5 were determined by a two-sided Pearson's correlation test.(D) The HCC individuals with low GLS or low SLC1A5 (filter by lower than the median expression) were used to analysis their prognosis basing on SREBF2 expression. (E) Model of HCC adapts to glutamine deprivation tumor microenvironment through lipophagy-induced cholesterol synthesis inhibition.
Fig 3: USP30 overexpression promotes SCC4 cell viability and glutamine consumption, and inhibits apoptosis through upregulation of c-Myc. A Cell viability, B, C apoptosis, D glutamine consumption, and E expression of GLS1 and SLC1A5 of SCC4 cells with USP30 overexpression and c-Myc inhibitor 10,058-F4 treatment. ***P < 0.001
Fig 4: NPs enhance the anticancer effects of MF-094 in HSC4 cells. A CLSM images (scale bars: 50 µm). B TEM images showing intracellular distribution of MF-094@NPs in HSC4 cells (scale bars: 4 µm). C Cell viability, D and E apoptosis, F glutamine consumption, and G expression of c-Myc, GLS1, and SLC1A5 in HSC4 cells incubated with MF-094, NPs, and MF-094@NPs. *P < 0.05, **P < 0.01, ***P < 0.001
Fig 5: PBX3 reversed the effect of miR-1294 on GC cell malignant phenotypes. (A–M) AGS and MKN-45 cells were introduced with miR-NC, miR-1294, miR-1294 + pcNDA, or miR-1294 + PBX3. (A) Cell proliferation, (B–D) cell migration and invasion, (E) and cell apoptosis were analyzed. (F, G) Western blot assay for apoptosis-related protein levels. (H) Tube formation ability, (I) glutamine level, (J) glutamate level, (K) and a-KG level were detected. (L, M) Detection of ASCT2 and GLS1 protein levels. *p < 0.05.
Supplier Page from Abcam for Anti-SLC1A5/ASCT2 antibody