Open Access

Butyrate upregulates the TLR4 expression and the phosphorylation of MAPKs and NK‑κB in colon cancer cell in vitro

  • Authors:
    • Tengfei Xiao
    • Shuiyun Wu
    • Cheng Yan
    • Chuanxiang Zhao
    • Huimin Jin
    • Nannan Yan
    • Jie Xu
    • Yi Wu
    • Ci Li
    • Qixiang Shao
    • Sheng Xia
  • View Affiliations

  • Published online on: July 24, 2018     https://doi.org/10.3892/ol.2018.9201
  • Pages: 4439-4447
  • Copyright: © Xiao et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Microbiota and its induced inflammation in colorectal mucosa have been considered risk factors for the development of colorectal carcinogenesis. Previous studies demonstrated that the coexisting elements of microbiota in the gut, such as short chain fatty acids (SCFAs) and lipopolysaccharides (LPS), which exhibited regulatory effects on the intestinal epithelial cells individually. Unfortunately, the association between butyrate and the toll‑like receptor (TLR) signaling pathway in the development of colon cancer is not fully elucidated. In the present study, by culturing human colon cancer SW480 cells or mouse colon cancer CT26 cells with butyrate and/or TLR4 ligand LPS in vitro, it was identified that butyrate suppressed the growth and promoted apoptosis of these cancer cells. Notably, the expression levels of TLR4 and CD14 were markedly increased on these butyrate‑treated cells, but not on LPS‑alone treated cells. Additionally, butyrate treatment induced the phosphorylation of extracellular signal‑regulated kinase, tumor protein 38, c‑Jun NH2‑terminal kinase and nuclear factor‑κB (NF‑κB) p65, and then promoted the pro‑inflammatory cytokine tumor necrosis factor‑α, but not interleukin 6 secretion in SW480 and CT26 cells. Therefore, butyrate treatment regulates the expression of TLR4, mitogen‑activated protein kinase and NF‑κB signal pathway activation and pro‑inflammatory response in vitro. Although the exact mechanisms have not been fully explored, these results suggested that butyrate and LPS‑TLR4 signaling mediated innate immunity in colon cancer cells through two distinct but inter‑regulated pathways. Thus, butyrate can further initiate innate immunity against tumor cells by upregulating the TLR4 expression and activation to preserve intestinal homeostasis.
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October-2018
Volume 16 Issue 4

Print ISSN: 1792-1074
Online ISSN:1792-1082

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Copy and paste a formatted citation
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Spandidos Publications style
Xiao T, Wu S, Yan C, Zhao C, Jin H, Yan N, Xu J, Wu Y, Li C, Shao Q, Shao Q, et al: Butyrate upregulates the TLR4 expression and the phosphorylation of MAPKs and NK‑κB in colon cancer cell in vitro. Oncol Lett 16: 4439-4447, 2018
APA
Xiao, T., Wu, S., Yan, C., Zhao, C., Jin, H., Yan, N. ... Xia, S. (2018). Butyrate upregulates the TLR4 expression and the phosphorylation of MAPKs and NK‑κB in colon cancer cell in vitro. Oncology Letters, 16, 4439-4447. https://doi.org/10.3892/ol.2018.9201
MLA
Xiao, T., Wu, S., Yan, C., Zhao, C., Jin, H., Yan, N., Xu, J., Wu, Y., Li, C., Shao, Q., Xia, S."Butyrate upregulates the TLR4 expression and the phosphorylation of MAPKs and NK‑κB in colon cancer cell in vitro". Oncology Letters 16.4 (2018): 4439-4447.
Chicago
Xiao, T., Wu, S., Yan, C., Zhao, C., Jin, H., Yan, N., Xu, J., Wu, Y., Li, C., Shao, Q., Xia, S."Butyrate upregulates the TLR4 expression and the phosphorylation of MAPKs and NK‑κB in colon cancer cell in vitro". Oncology Letters 16, no. 4 (2018): 4439-4447. https://doi.org/10.3892/ol.2018.9201