Previous reports indicate that the beneficial effect of chitin nanofibrils (CNFs), and chitosan nanofibrils (CSNFs) for wound healing. In this study, the wound healing effects of superficially deacetylated chitin nanofibrils (SDACNFs) were evaluated using an experimental model. In the experiments using circular excision wound model, SDACNFs induced re-epithelium and proliferation of the fibroblasts and collagen tissue. In the chitin, CNFs, and CSNFs, on the other hand, the e-epithelium and proliferation of the fibroblasts and collagen tissue were not induced perfectly compared with the SDACNFs group. In particular, re-epithelization was observed on day 4 in the only SDACNF group. Moreover, SDACNFs did not induce severe systemic inflammation in the linear incision wound model. The data indicated that SDACNFs effectively induced the proliferation and re-modeling phases compared with chitin, CNFs, and CSNFs in the wound. These data indicate that SDACNFs can be beneficial as a new biomaterial for wound healing.

This study investigated the prophylactic effects of orally administered surface-deacetylated chitin nanofibers (SDACNFs) and chitosan against 5-fluorouracil (5-FU)-induced intestinal mucositis, which is a common side effect of 5-FU chemotherapy. SDACNFs and chitosan abolished histological abnormalities associated with intestinal mucositis and suppressed hypoproliferation and apoptosis of intestinal crypt cells. These results indicate that SDACNF and chitosan are useful agents for preventing mucositis induced by anti-cancer drugs.

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Microscopic surface architectures that can be easily manufactured have been in demand as mechano-structural cues for tissue engineering. Microscopic surface reliefs synthesized by wrinkling were expected as cell culture scaffolds for cell proliferation, control of cellular alignment and differentiation, and spheroid generation. We previously developed bio-based wrinkled films prepared via lignification-mimetic reactions and drying. Although these films are expected as a candidate for cell culture scaffolds, stability and morphology of the wrinkled surfaces in aqueous buffer solutions were not explored. Here, we investigate the surface morphologies of the wrinkled films in phosphate-buffered saline, and their application to 3T3 cell culture. The wrinkled film prepared with the immersion treatment at 40 • C maintained its wrinkled structure in phosphate-buffered saline even after five days, although the wrinkles were broadened by hydration of the skin layer. Interestingly, higher cell numbers were observed in the 3T3 cell culture using the wrinkled film than using flat film with the same surface composition. In addition, the high biocompatibility of the wrinkled film was confirmed by in vivo experiments. These results strongly encourage application of the wrinkled film as a mechano-structural cue. Studies of the advanced applications for the wrinkled films are now in progress.

Cancer‐associated fibroblasts (CAFs) are a major component of the tumor microenvironment that mediate resistance of cancer cells to anticancer drugs. Tranilast is an antiallergic drug that suppresses the release of cytokines from various inflammatory cells. In this study, we investigated the inhibitory effect of tranilast on the interactions between non–small cell lung cancer (NSCLC) cells and the CAFs in the tumor microenvironment. Three EGFR‐mutant NSCLC cell lines, two KRAS‐mutant cell lines, and three CAFs derived from NSCLC patients were used. To mimic the tumor microenvironment, the NSCLC cells were cocultured with the CAFs in vitro, and the molecular profiles and sensitivity to molecular targeted therapy were assessed. Crosstalk between NSCLC cells and CAFs induced multiple biological effects on the NSCLC cells both in vivo and in vitro, including activation of the STAT3 signaling pathway, promotion of xenograft tumor growth, induction of epithelial‐mesenchymal transition (EMT), and acquisition of resistance to molecular‐targeted therapy, including EGFR‐mutant NSCLC cells to osimertinib and of KRAS‐mutant NSCLC cells to selumetinib. Treatment with tranilast led to inhibition of IL‐6 secretion from the CAFs, which, in turn, resulted in inhibition of CAF‐induced phospho‐STAT3 upregulation. Tranilast also inhibited CAF‐induced EMT in the NSCLC cells. Finally, combined administration of tranilast with molecular‐targeted therapy reversed the CAF‐mediated resistance of the NSCLC cells to the molecular‐targeted drugs, both in vitro and in vivo. Our results showed that combined administration of tranilast with molecular‐targeted therapy is a possible new treatment strategy to overcome drug resistance caused by cancer‐CAF interaction.