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Fig. 5 | Journal of Experimental & Clinical Cancer Research

Fig. 5

From: Essential role for STAT3/FOXM1/ATG7 signaling-dependent autophagy in resistance to Icotinib

Fig. 5

Chloroquine and STAT3/FOXM1 signalling blockade effectively sensitize EGFR-mutated NSCLC cells to icotinib in vivo. A Tumours were excised and collected after treatment with icotinib/CQ alone or the combination for 21 days. B-D Tumour weight (B), tumour volume (C), and body weight (D) of indicated xenografts are shown. E Immunoblotting assays measured LC3 conversion and the expression of STAT3, FOXM1, and ATG7. F Paraffin-embedded sections of tumour tissues from xenografted mice were analyzed by TUNEL staining. Scale bar: 10 μm. G Ultrastructural changes of autophagic vesicles and apoptotic bodies in tumour tissues of indicated xenografts are shown. Scale bar: 1 μm. P, phagosome. AP, autophagosome. AL, autolysosome. AC, apoptotic cell. AB, apoptotic body. ER, endoplasmic reticulum. M, mitochondrion. Golgi, golgi apparatus. H Xenograft tumours were excised from the group of icotinib, LV-STAT3-Y705F and shFOXM1 alone or combination. I-K) Tumour weight (I), tumour volume (J), and growth curve (K) of indicated xenografts are shown. [**P < 0.01, ***P < 0.001, ns, no significance as compared with the control group. #P < 0.05, ###P < 0.001 as compared with the icotinib alone group. ζP < 0.05, ζζζP < 0.001 as compared with icotinib plus LV-STAT3WT, ξP < 0.05, ξξP < 0.01 as compared with icotinib plus shNC. ††P < 0.01, †††P < 0.001 as compared with icotinib plus LV-STAT3-Y705F. φφP < 0.01, φφφP < 0.001 as compared with icotinib plus shFOXM1]

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