Fig. 7: E7-circp53-EVs and Her2-circp53-EVs selectively inhibit tumor growth in PDX and NOD/SCID-TIBIA mouse models.

a, An IVIS spectrum was recorded to show the high fluorescence intensity in the spine and prolonged retention time in the E7-circp53-EVs group, further confirming its ability to target bone in vivo. b, Images of NOD/SCID-TIBIA mice in NC, circp53-EVs and E7-circp53-EVs groups. c, Human κFLC levels in mouse serum were measured by an ELISA. d, Representative micro-computed tomography images of bones in the NC, circp53-EVs and E7-circp53-EVs groups. e, The BMD of NOD/SCID-TIBIA mice in the NC, circp53-EVs, and E7-circp53-EVs groups. f, The BV/TV of NOD/SCID-TIBIA mice in the NC, circp53-EVs and E7-circp53-EVs groups. g, h, Images of PDX model mice on day 27 (g) and tumors taken from mice in each group (h) (P < 0.001). i, Tumor growth curves of the PDX model for the NC, circp53-EVs and Her2-circp53-EVs groups. j, Tumor weights of the PDX model in the NC, circp53-EVs and E7-circp53-EVs groups. k, IVIS was employed to observe the fluorescence in the NC, circp53-EVs and E7-circp53-EVs groups. l, RT–qPCR analysis revealed that Her2-circp53-EVs accumulated to a greater extent in PDX tumors compared with other organs such as the heart, liver, spleen, lung and kidney. m, Confocal imaging of EVs biodistribution in murine organs. n, Confocal microscopy of frozen sections showed that Her2-circp53-EVs accumulated to a greater extent in PDX tumors compared with other organs such as the heart, liver, spleen, lung and kidney by quantitative statistics. The data are presented as mean ± s.d. (n = 6 mice for each group, ^*P < 0.05, ^**P < 0.01, ^***P < 0.001 and ns, no statistical significance).