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. 2024 Feb 4;15(6):1750–1761. doi: 10.7150/jca.91089

Figure 4.

Figure 4

B7-H3 directly activated EGFR-ERK signaling to promote chemoresistance. A. Knockdown of B7-H3 significantly decreased the level of phosphor-ERK and increased the cleavage of caspase-3 in response to OXP treatment (30μM, n=3). B. Knockdown of B7-H3 significantly decreased the cell viability in response to OXP treatment (30 μM, n=3). One-Way ANOVA analysis. **p<0.01 and ***p<0.001. C. LoVo cells were transfected with pCMV-EGFR-flag for 24 hr and treated with OXP (30 μM) and anti-B7-H3 antibodies for 24 hr. The expression of p-ERK1/2 and cleaved casp.3 was analyzed by immunoblotting. D. LoVo cells were transfected with pCMV-EGFR-flag for 24 hour and treated with OXP (30 μM) and anti-B7-H3 antibodies for 24 hr. The activity of Casp.3 was analyzed by caspase-3 activity kit (n=3). *p<0.05, **p<0.01 and ***p<0.001. E. LoVo cells were transfected with pCMV-B7-H3-flag for 24 hr and treated with OXP (30 μM) and gefitinib (30 μM) for 24 hr. Cell viability was determined by CCK8 assay (n=3). *p<0.05 and **p<0.01. F. LoVo cells were transfected with pCMV-B7-H3-flag for 24 hr and treated with OXP (30 μM) and gefitinib (30 μM) for 24 hr. Cell death was determined by caspase-3 activity assay (n=3). *p<0.05 and ***p<0.001.