4.7 Article

Targeting aberrant colon cancer-specific DNA methylation with lipoteichoic acid-deficient Lactobacillus acidophilus

期刊

GUT MICROBES
卷 4, 期 1, 页码 84-88

出版社

TAYLOR & FRANCIS INC
DOI: 10.4161/gmic.22822

关键词

colorectal cancer; aberrant epigenetic alterations; DNA methylation; lipoteichoic acid; inflammation

资金

  1. NIH [1R01AI098833-01]
  2. DoD [CA111002]
  3. NIH/NCRR Clinical and Translational Science Award [UL1 RR029890]

向作者/读者索取更多资源

Pathogenic autoinflammatory responses triggered by dysregulated microbial interactions may lead to intestinal disorders and malignancies. Previously, we demonstrated that a lipoteichoic acid (LTA)-deficient Lactobacillus acidophilus strain, NCK2025, ameliorated inflammation-induced colitis, significantly reduced the number of polyps in a colonic polyposis cancer model and restored physiological homeostasis in both cases. Nonetheless, the regulatory signals delivered by NCK2025 to reprogram the gastrointestinal microenvironment, and thus resist colonic cancer progression, remain unknown. Accumulating evidence suggest that epigenetic changes, in the presence and absence of pathogenic inflammation, can result in colorectal cancer (CRC). To test possible epigenetic modifications induced by NCK2025, the expression of epigenetically regulated, CRC-associated genes was measured with and without bacterial treatment. In vivo and in vitro, NCK2025 enhanced the expression of tumor suppressor genes that may regulate CRC development. Therefore, differential epigenetic regulation of CRC-related genes by NCK2025 represents a potential therapy against colitis-associated and sporadic CRC.

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