Fig. 2

eMSCs suppressed the malignant behaviors of EC cells. A CM derived from eMSCs showed the most significant anti-proliferative effect on EC cells, compared to AD-MSCs and UC-MSCs. RL95-2 and HEC-1A cells were treated with NM or CM derived from MSCs for 48 h before Cell Viability Assay. B CM derived from eMSCs markedly increased BAX expression and BAX/BCL2 ratio and decreased BCL2 expression in EC cells, compared to AD-MSCs and UC-MSCs. RL95-2 and HEC-1A cells were treated with NM or CM derived from MSCs for 48 h before western blotting. BAX/BCL2 ratio was calculated from densitometry by ImageJ. C RL95-2 and HEC-1A cells seeded in 24‐well chambers were co-cultured with or without MSCs, as shown in the pattern diagram for 24 h before cell migration assay. D eMSCs did not affect EC cell migration, while AD-MSCs promoted EC cell migration. UC-MSCs slightly induced migration of HEC-1A cells but had no effect on RL95-2 cells. Bright field images were taken (Left), and the numbers of migratory cells per bright field image were calculated (Right). Original magnification 4 × ; Scale bar, 400 μm. E–G eMSCs had the highest inhibitory effect on EC xenograft tumor growth, compared to AD-MSCs and UC-MSCs. RL952 cells alone, or RL95-2 cells and MSCs (5:1) were subcutaneously injected in female nude mice. Mice were sacrificed after 28 days (E), tumor tissues were photographed (F), and tumor weight was then measured (G). H-I H&E and IHC staining images for Ki67 in xenograft tumors. NM, normal medium; CM, conditioned medium; The blots of BAX, BCL2, and GAPDH were all cropped (B) and full-length blots were presented in Additional file 7: Fig. S6. Data were analyzed by ratio t-test (A) and unpaired t-test (B, D, G, and I). ns, not significant; *P < 0.05; **P < 0.01; ***P < 0.001