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Fig. 3 | Journal of Experimental & Clinical Cancer Research

Fig. 3

From: Unveiling CXCR2 as a promising therapeutic target in renal cell carcinoma: exploring the immunotherapeutic paradigm shift through its inhibition by RCT001

Fig. 3

RCT001 inhibits angiogenesis and viability of primary RCC cells in vitro. a Immunoblot analysis of pERK1/2 expression in serum-depleted endothelial cells determined 24 h after stimulation by CXCL8 (75 ng/mL) and/or treatment with RCT001 (1 μM). b Matrigel-based tube formation assay was performed with endothelial cells 4 h after treatment with RCT001 (0.1 or 0.5 μM). c. Wound scratch assay was performed with serum-depleted endothelial cells treated or not with CXCL8 (75 ng/mL) in the presence of RCT001 (0.1, 0.2 or 0.5 μM). Wound closure was determined 4 and 8 h after treatment. d-e Cell proliferation assay of serum-depleted endothelial cells treated or not with CXCL7 (75 ng/mL) (d) or CXCL8 (75 ng/mL) (e) in the presence of RCT001 (0.1, 0.2 or 0.5 μM) for 72 h. f Clonogenic assay with two primary RCC cells in the presence or not of RCT001 (1 or 2.5 μM). g Viability of two primary RCC cells treated with RCT001 for 48 h. h Evaluation of CXCL1/5/8 and VEGFA mRNA levels in primary RCC cells after 24 h of treatment with RCT001 treatment (1 or 2.5 μM) by qPCR. Results are presented as the mean of three independent experiments ± SD. Statistics were performed using the ANOVA test: **p < 0.01, *** p < 0.001 vs control conditions, #p < 0.01, ###p < 0.001 vs CXCL8 conditions

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