Figure 4
Figure 4. IGF-1R inhibitor inhibited the effect of IL-6, HGF, and HB-EGF, unlike that of APRIL. (A) HMCLs were starved for 2 hours and cultured without cytokine or with either IL-6 (200 pg/mL) or IGF-1 (100 ng/mL) or APRIL (200 ng/mL) or HGF (20 ng/mL) or HB-EGF (1 μg/mL) and without inhibitor or with anti–IL-6 mAb (10 μg/mL) or IGF-1R inhibitor (1 μM) or pan-ErbB kinase inhibitor (1 μM) or anti-HGF mAb (25 μg/mL) or BCMA-Fc (10 μg/mL) for 4 days in the Syn H culture medium. The cell concentrations were 2 × 105 cells/mL for XG-1 and XG-2 HMCLs and 105 cells/mL for XG-5, XG-7, and XG-20 HMCLs. Results are the mean luminescent signals ± SD determined in sextuplicate culture wells and are those of 1 experiment representative of 3. Data are expressed as percentage of the signal obtained with the growth factor. *The mean value was significantly different from that obtained in the control group using a Student t test (P ≤ .05). XG-5 HMCL was only stimulated by IGF-1 (2.8-fold), XG-20 HMCL by IL-6 (2.9-fold), or IGF-1 (3.5-fold), XG-7 HMCL by IL-6 (2.2-fold), IGF-1 (2.3-fold), or HGF (2.7-fold), XG-1 HMCL by IL-6 (11-fold), IGF-1 (5-fold), or APRIL (5-fold), and XG-2 by IL-6 (11-fold), IGF-1 (17-fold), HGF (17-fold), or HB-EGF (2-fold). (B) HMCLs were starved for 2 hours and cultured without cytokine or with IL-6 (200 pg/mL) or IGF-1 (100 ng/mL) and without inhibitor or with an anti–IL-6 mAb (10 μg/mL) or an IGF-1R inhibitor (1 μM) for 4 days in the Syn H culture medium. Data are expressed as the mean percentage of the inhibition of the cytokine stimulation by the inhibitor in 3 independent experiments. When the percentages were different with a Student t test for pairs (P ≤ .05), data are shown in bold and italic. NS indicates not stimulated.

IGF-1R inhibitor inhibited the effect of IL-6, HGF, and HB-EGF, unlike that of APRIL. (A) HMCLs were starved for 2 hours and cultured without cytokine or with either IL-6 (200 pg/mL) or IGF-1 (100 ng/mL) or APRIL (200 ng/mL) or HGF (20 ng/mL) or HB-EGF (1 μg/mL) and without inhibitor or with anti–IL-6 mAb (10 μg/mL) or IGF-1R inhibitor (1 μM) or pan-ErbB kinase inhibitor (1 μM) or anti-HGF mAb (25 μg/mL) or BCMA-Fc (10 μg/mL) for 4 days in the Syn H culture medium. The cell concentrations were 2 × 105 cells/mL for XG-1 and XG-2 HMCLs and 105 cells/mL for XG-5, XG-7, and XG-20 HMCLs. Results are the mean luminescent signals ± SD determined in sextuplicate culture wells and are those of 1 experiment representative of 3. Data are expressed as percentage of the signal obtained with the growth factor. *The mean value was significantly different from that obtained in the control group using a Student t test (P ≤ .05). XG-5 HMCL was only stimulated by IGF-1 (2.8-fold), XG-20 HMCL by IL-6 (2.9-fold), or IGF-1 (3.5-fold), XG-7 HMCL by IL-6 (2.2-fold), IGF-1 (2.3-fold), or HGF (2.7-fold), XG-1 HMCL by IL-6 (11-fold), IGF-1 (5-fold), or APRIL (5-fold), and XG-2 by IL-6 (11-fold), IGF-1 (17-fold), HGF (17-fold), or HB-EGF (2-fold). (B) HMCLs were starved for 2 hours and cultured without cytokine or with IL-6 (200 pg/mL) or IGF-1 (100 ng/mL) and without inhibitor or with an anti–IL-6 mAb (10 μg/mL) or an IGF-1R inhibitor (1 μM) for 4 days in the Syn H culture medium. Data are expressed as the mean percentage of the inhibition of the cytokine stimulation by the inhibitor in 3 independent experiments. When the percentages were different with a Student t test for pairs (P ≤ .05), data are shown in bold and italic. NS indicates not stimulated.

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