Fig. 7

ANXA1 inhibiting combine with glutamine deficiency suppress tumor cells growth and proliferation. A: Immunofluorescence co-localization of ANXA1 and GOT1 in HUCCT1 cells cultured in CM or Gln (-). B: CCK8 proliferation assay was used to detect the proliferation ability of HUCCT1 cells treated with sh-Ctrl、sh-ANXA1#1、sh-ANXA1#1 + oe-GOT1 in complete medium (CM) and glutamine-deficient Gln (-) medium. C: Plate cloning was used to detect the proliferation ability of HUCCT1 cells treated with sh-Ctrl、sh-ANXA1#1、sh-ANXA1#1 + oe-GOT1 in complete medium (CM) and glutamine-deficient (Gln (-)) medium. D: EDU assay was used to detect the proliferation ability of HUCCT1 cells treated with sh-Ctrl、sh-ANXA1#1、sh-ANXA1#1 + oe-GOT1 in complete medium (CM) and glutamine-deficient (Gln (-)) medium. E:Levels of ROS and GSH was detected in HUCCT1 cells in complete medium (CM) and glutamine-deficient (Gln (-)) medium. F: Different groups of stable cell lines were transplanted subcutaneously into nude mice and raised with or without glutamine. G: HUCCT1 cells of sh-Ctrl, sh-ANXA1#1, sh-ANXA1#1 + oe-GOT1 were subcutaneously inoculated into nude mice fed with glutamine diet or lacking glutamine diet. H: The corresponding tumor volume growth curve and weight are shown. I: GSH or ROS levels were examined in CDX with stable of knockdown ANXA1 or overexpress GOT1. Data are representative of three (B, C, D, H(left)) or five (H(right), I) independent experiments. One-way ANOVA (C, D, E, H(right), I); Two-way ANOVA (B, H(left)). **, p < 0.01; ***, p < 0.001. Data are mean ± SD