Fig. 6

FBN1 knockout inhibits progression of ovarian cancer and sensitizes response to cisplatin in vivo. (A) Images of tumors generated by FBN1‐knockout and control cisplatin‐resistant ovarian cancer organoids with or without cisplatin and/or apatinib. (B) Growth curves of xenograft tumors in mice. (C) Average tumor weights in nude mice. (D) Representative images of PET‐CT used for detection of glucose uptake. Each group contained 5 mice. (E) Average SUVmax values of nude mice bearing tumors. (F) Effect of FBN1 morpholino in zebrafish model was tested by qRT‐PCR. (G) Zebrafish model treated with or without cisplatin (0.2 mmol/L) and/or apatinib (40 μmol/L). (H) VEGFA mRNA in zebrafish models. (I) Immunofluorescence of FBN1 and specific angiogenesis marker CD31 in the xenograft tumors of FBN1 knockout and control groups with cisplatin treatment. (J) qRT‐PCR analysis of the indicated genes in FBN1‐knockout group and the control in nude mouse tumor tissues without drug treatment. Error bars, 95% CIs. *, P < 0.05, **, P < 0.01. (K) Heatmap showing that FBN1‐affected genes are involved in glycolysis and angiogenesis with cisplatin treatment. Abbreviations: FBN1, fibrillin‐1; CR, cisplatin‐resistant; KO, knockout; NC, negative control; OE, overexpression; VEGFA, vascular endothelial growth factor A; qRT‐PCR, quantitative real‐time PCR; CD31, platelet endothelial cell adhesion molecule‐1