Fig 1: IL-17B induce the expression of IL-17RB, the underlying mechanism of which is not clear.The binding between IL-17B and IL-17RB recruits TRAF6 in cytoplasm to induce the K63-linked ubiquitination of Beclin-1, which leads the autopahagosome formation, to further reinforce the self-renewal and tumorigenesis ability of CSCs.
Fig 2: IL-17B promoted self-renewal and expansion of CSCs depending on IL-17RB.A Representative images of MGC-803 cells cultured in serum-free medium for 7 days and stimulated by rIL-17B or PBS. B Statistical analysis of the spheroid number (diameter > 50 μm) according to figure subpart A (n = 6; ***p < 0.001). C–E Flow cytometric analysis of the expression of Lgr5, CD133, and CD90 in MGC-803 cells treated with different concentrations of rIL-17B (n = 3; ***p < 0.001). F, G qRT-PCR was performed to detect the expression of CK18 and MUC1 in MGC-803 cells treated with different concentrations of rIL-17B (n = 3; **p < 0.01; ***p < 0.001). H Representative images showing the general number and size of spheroids in MGC-803 cells infected with shIL-17RB or shControl lentiviral vectors and stimulated with different concentrations of rIL-17B for 7 days. I Statistical analysis of the number of spheroids (diameter > 50 μm) based on figure subpart H (n = 6; ***p < 0.001).
Fig 3: rIL-17B promoted autophagy activation and ubiquitination of Beclin-1 by inducing IL-17RB expression.A The relationship between IL-17B in the serum and the expression of IL-17RB mRNA in GC tissues from the same patient. B qRT-PCR was used to detect IL-17RB mRNA expression in MGC-803 cells treated with rIL-17B or PBS for 48 h (n = 3; ***p < 0.001). C Immunofluorescence was used to assay the IL-17RB protein expression in MGC-803 cells treated with rIL-17B or PBS for 48 h. D After transfection with different concentrations of Flag-IL-17RB and HA-Beclin-1 (2 μg) plasmids, 293T cells were subjected to IP using an HA antibody or control IgG, followed by IB with K63-linked ubiquitin, IL-17RB, Beclin-1, and GAPDH antibodies. E After transfection with different concentrations of Flag-IL-17RB, HA-Beclin-1, and MYC-TRAF6 plasmids, 293T cells were subjected to IP using an HA antibody or control IgG, followed by IB with HA, MYC, and IL-17RB antibodies. F Deletion of the TRAF6-binding domain in IL-17RB (Flag-IL-17RB△) abolished recruitment and binding between TRAF6 and Beclin-1.
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