{'fraction_non_alphanumeric': 0.029048656499636893, 'fraction_numerical': 0.00944081336238199, 'mean_word_length': 5.4392523364485985, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Axitinib, a selective inhibitor of vascular endothelial growth factor receptor, exerts an anticancer effect in melanoma through promoting antitumor immunity

In this study, we investigated the antitumor activity of axitinib, a selective inhibitor of vascular endothelial growth factor receptor tyrosine kinases, against melanoma cells. Axitinib dose-dependently inhibited the proliferation and induced the apoptosis of B16F1 cells in vitro. In a mouse model of melanoma xenograft, axitinib significantly suppressed tumor growth and induced apoptosis of cells in tumor tissues at a dose of 25 mg/kg. In addition, axitinib suppressed the lung metastasis of melanoma cells and prolonged the life span of tumor-bearing mice. Axitinib also enhanced the proportion of CD8+ T cells and reduced the proportion of myeloid-derived suppressor cells in CD45.2+ cells, whereas the proportions of CD4+ T cells and Treg cells were not affected. The mRNA expressions of inducible nitric oxide synthases-2 and arginase-1, which were associated with the function of myeloid-derived suppressor cells in tumor tissues, were inhibited by axitinib. Moreover, axitinib suppressed the expressions of proinflammatory cytokines such as IL-6, TNF-&agr;, and IFN-&ggr;. Altogether, our results showed the unique antitumor mechanism of axitinib and provided useful information for its clinical application.