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Fig. 8 | Journal of Experimental & Clinical Cancer Research

Fig. 8

From: The U2AF2 /circRNA ARF1/miR-342–3p/ISL2 feedback loop regulates angiogenesis in glioma stem cells

Fig. 8

The U2AF2/circARF1/miR-342–3p/ISL2 feedback loop promoted glioma tumorigenesis and angiogenesis. a Representative images show the size of intracranial tumors in the coronal location of eight groups (negative control, ISL2 overexpression, miR-342–3p mimic, ISL2 overexpression combined with miR-342–3p mimic, cARF1 knockdown, ISL2 overexpression combined with cARF1 knockdown, U2AF2 overexpression, and cARF1 knockdown combined with U2AF2 overexpression in GSC406). Scale bar = 10 mm. b The measured tumor volumes among eight GSC406 groups are indicated. c Kaplan-Meier survival curves showed that ISL2 overexpression, U2AF2 overexpression, and ISL2 overexpression combined with the miR-342–3p mimic in GSC406 cells shortened the survival times of nude mice, while it prolonged the survival times after the miR-342–3p mimic was transfected, cARF116 knockdown, and U2AF2 overexpression combined with cARF116 knockdown in GSC406 cells. For each group, n = 5. d, e Representative immunohistochemical staining showing the changes in ISL2, U2AF2, VEGFA, and CD31 in the negative control, ISL2 overexpression, miR-342–3p mimic, ISL2 overexpression combined with miR-342–3p mimic, cARF1 knockdown, ISL2 overexpression combined with cARF1 knockdown, U2AF2 overexpression, and cARF1 knockdown combined with U2AF2 overexpression orthotopic xenograft models. Scale bar = 50 μm. f The microvessel density (MVD) with mouse specific CD31 staining in tumor tissues were counted. g Schematic diagram showing that the U2AF2/cARF1/miR-342–3p/ISL2 axis promoted glioma tumorigenesis and angiogenesis through VEGFA-mediated ERK signaling pathway. #p < 0.05 vs. the negative control group, &p < 0.05 vs. the miR-342–3p mimic group, §p < 0.05 vs. the cARF1 knockdown group, p < 0.05 vs. the U2AF2 overexpression group. EV: empty vector, OE: overexpression, NC: negative control, KD: knockdown

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