Fig. 7: S100A4 promoted lung tumor development by inhibiting autophagy.
From: S100A4 promotes lung tumor development through β-catenin pathway-mediated autophagy inhibition
Groups of C57BL/6 mice and S100A4−/− mice (n = 9 per group) were subcutaneously injected with 1 × 106 LLC cells. a The survival analysis of lung tumor-bearing mice. b Tumor volumes were monitored every other day. Representative data from three independent experiments are shown. c On day 20 after tumor inoculation, mice were killed and tumors from the two groups are shown. d The tumor sections were stained for S100A4 and Ki67. Scale bar, 50 μm. HPF high power field. e Representative H&E-stained lung sections of WT and S100A4−/− mice. The percentage of the metastatic area was quantified using Image-Pro Plus (IPP). f The levels of the autophagy-related proteins p62, Beclin1 and LC3-I/II in tumors from WT and S100A4−/− mice were detected by western blot. g mRNA expression of Beclin1, LC3-I/II, p62 and ATG5 in tumors from S100A4−/− and WT mice was detected by real-time PCR. h Representative electron microscopy of dissected tumors from S100A4−/− and WT mice. Scale bar, 0.25 μm. i Schematic of the S100A4 acting model in lung cancer. S100A4 is a negative regulator of autophagy via activation of the β-catenin signaling pathway and this process is RAGE dependent. The autophagy inhibitor S100A4 contributed to lung tumor cell growth; *p < 0.05, **p < 0.01
