Anti-tumor Mechanisms of Short-chain Fatty Acids, and the Relationship between the Gut Microbiome, Carcinogenesis, Tumor Growth, and Proliferation in Colorectal Carcinoma

T. Ohara, Y. Taki
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Abstract

Short-chain fatty acids (SCFAs) produced by the gut microbiome have been reported to have anti-tumor effects in several experimental systems [1-3]. Previously, we investigated the inhibitory effects of SCFAs (butyric acid, isobutyric acid, and acetic acid) on cell growth and proliferation in cultured human colorectal carcinoma (CRC) cell lines (DLD-1 cells, WirDr cells), and found that butyric acid displayed the strongest inhibitory effect [4]; however, the underlying mechanisms have not yet been elucidated. To investigate the anti-tumor mechanisms of SCFAs, we performed an in silico analysis of their inhibitory mechanism on tumor cell growth and proliferation in an experimental system in which SCFAs were added to cultured human CRC cell lines [5]; the results revealed that SCFAs suppress genes and transcription factors that participate in tumor cell growth, proliferation, and turnover, but do not affect genes involved in carcinogenesis, or genomes and factors associated with carcinogenic pathways.
短链脂肪酸的抗肿瘤机制以及肠道微生物群与结直肠癌癌变、肿瘤生长和增殖的关系
据报道,肠道微生物组产生的短链脂肪酸(SCFAs)在几个实验系统中具有抗肿瘤作用[1-3]。此前,我们研究了SCFAs(丁酸、异丁酸和乙酸)对培养的人结直肠癌(CRC)细胞系(DLD-1细胞、WirDr细胞)细胞生长和增殖的抑制作用,发现丁酸的抑制作用最强[4];然而,潜在的机制尚未阐明。为了研究SCFAs的抗肿瘤机制,我们在实验系统中对SCFAs对肿瘤细胞生长和增殖的抑制机制进行了计算机分析,该实验系统将SCFAs添加到培养的人CRC细胞系中[5];结果显示,SCFAs抑制参与肿瘤细胞生长、增殖和更新的基因和转录因子,但不影响致癌基因,也不影响与致癌途径相关的基因组和因子。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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