Fig 1: CRART16 promotes angiogenesis and bevacizumab resistance by regulating the miR-122-5p/c-Fos axis. (A) Effects of conditioned medium on spheroid sprouting of HUVECs (*P < 0.05). (B) Effects of indicated conditioned medium on capillary formation by HUVECs (*P < 0.05). (C) The apoptosis rate of indicated cells treated with bevacizumab for 48 hours (*P < 0.01). (D) Levels of c-Fos and VEGFD were determined by western blotting. GAPDH served as a loading control (*P < 0.05). The expression levels of VEGFD in conditioned media from different kinds of gastric cancer cells were determined by ELISA (*P < 0.05). (E) Based on western blotting, the relative expression levels of cleaved caspase-3 and cleaved PARP in indicated gastric cancer cells treated with bevacizumab for 48 hours. ß-Actin served as a loading control (*P < 0.05). All data are presented as mean ± SD from three separate experiments.
Fig 2: CRART16 overexpression in gastric cancer cells accelerates tumor growth and upregulates angiogenesis in nude mouse models. (A) Tumor volumes and tumor weights are illustrated as mean ± SD for six mice from different groups (*P < 0.05). (B) Representative micrographs and quantitation of immunostaining against c-Fos, VEGFD, and CD31 in different tumor sections. All data are presented as mean ± SD of quintuplicate determinations of six mice from different groups (**P < 0.01).
Fig 3: CRART16 overexpression increases c-Fos and VEGFD expression by targeting miR-122-5p. (A) The relative levels of miR-122-5p and mRNAs encoding FOS and VEGFD in different gastric cancer cell lines were analyzed by qRT-PCR (*P < 0.05). (B) The relative levels of c-Fos and VEGFD in different gastric cancer cell lines were determined by western blotting. GAPDH was used as a loading control (*P < 0.05). (C) The expression levels of VEGFD in conditioned media from different types of gastric cancer cells were determined by ELISA (**P < 0.01). All data are presented as mean ± SD from three separate experiments.
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