Since the 1980s, there have been numerous reports on the antitumor activity of COS and its mechanism. Among them, chitohexaose is the most studied. In 1986, Suzuki et al reported that N-acetylchitohexaose and chitohexaose can highly inhibit the growth of sarcoma 180 and MM-46 solid tumors transplanted in mice. In 1988, Tokoro et al. found in a follow-up study that N-acetylchitohexaose and chitohexaose also inhibited the growth of methamphetamine solid tumor transplantation in BALB/c mice, but the lower homologue N-acetylchitohexaose And chitosan can not show the same effect. Therefore, N-acetylchitohexaose and chitohexaose correspond to 6 GlcNAc residues and GlcN residues, respectively, and their molecular size can be regarded as one of the necessary factors to show their antitumor effects. This was further confirmed by the study of Xiong Chuannan et al. in 2009. Compared with other chitosan oligosaccharide monomers (chitobiose, chitotriose, chitotetraose, and chitopentaose), chitohexaose was effective in tumor-induced ECV304 cells. It has a strong inhibitory effect on the proliferation and migration of ECV304 cells. Studies have shown that chitohexaose can down-regulate the expression of VEGF and uPA mRNA in ECV304 cells. In 2011, Li Xian et al. studied the effect of chitohexaose on the regulation of cyclin D1, bcl-2 and bcl-xl mRNA levels in A549 cells, and found that chitohexaose also significantly down-regulated the mRNA levels that are mainly involved in inhibiting tumor cell proliferation and tumor cell apoptosis. The expression levels of cyclin D1 and bcl-xl mRNA further indicated that chitohexaose had the strongest inhibitory effect on the proliferation of A549 cells.
The content is selected from "Advances in preparation, analysis and biological activities of single chitooligosaccharides" by Li Kecheng
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