Fig. 6: Inflammation and IL-6 triggered by paclitaxel exposure facilitate tumor growth and modification of the tumor microenvironment in vivo.

A Tumor-proliferation curve. Inflammation attenuation and IL-6R blocking (with tocilizumab) enhanced the tumor-proliferation inhibition of paclitaxel (PTX). B Histology features (a-g) and PGCC percentage (h) of tumor in each group. Compared with the control (1.8 ± 0.7%), PGCCs were significantly induced by PTX alone (14.6 ± 5.4%, P < 0.05), which was attenuated by combined administration of PTX with tocilizumab (5.2 ± 2.1%, P < 0.05) and/or apigenin (4.8 ± 1.9%, P < 0.05), but tocilizumab or apigenin alone had no significant effect. H&E staining, bars, 50 µm. a, control; b, tocilizumab; c, apigenin; d, PTX; e, PTX + tocilizumab; f, PTX + apigenin; g, PTX + tocilizumab + apigenin. C PTX can significantly lower the tumor/stroma ratio (Control, 6.3 ± 2.9; PTX, 1.9 ± 0.5), which can be enhanced by tocilizumab (0.8 ± 0.5) and apigenin (1.2 ± 0.5). D Microvessel density in tumor increased significantly in the subgroups of PTX (23 ± 5.5 per area of 500 µm diameter), PTX + tocilizumab (14.5 ± 3.9), PTX + apigenin (14.3 ± 3.6), and PTX + tocilizumab + apigenin (12.1 ± 3.2). IL-6R blocking and apigenin reduced the effect of PTX alone when combined together with PTX.