Fig. 7

Co-delivery of aPKCι-siRNA and GEM via liposomes for the effective treatment of CCA. A. Anchorage-independent growth of CCA cells in soft agar in the presence of si-NC-L, aPKCι-siRNA-L, GEM, GEM-aPKCι-siRNA, GEM-L, GEM-aPKCι-siRNA-L compared with that of cells in the presence of PBS alone. B. Schematic demonstrating the method for the analysis of the antitumor effect in human CCA cell xenografts. C. The tumor volume (left) and representative images (right) of xenograft tumors are shown from different groups. Data represent the mean ± SEM. *P < 0.05, ***P < 0.001. D. Immunohistochemical staining of aPKCι, F4/80 and NF-κB protein in tumor tissue in various treatment groups. Scale bar, 200 μm. E. The structure and antitumor mechanisms of GEM-aPKCι-siRNA-L. F. Schematic illustration of the proposed Macrophages-aPKC_ɩ-CCL5 feedback loop involved in the regulation of cholangiocarcinoma progression and improvement in chemotherapeutic responses