Toll-like Receptor 4 Activation Increases Akt Phosphorylation in Colon Cancer Cells

被引：1
作者：
Doan, Hung Q. [1 ]
Bowen, Kanika A. [1 ]
Jackson, Lindsey A. [1 ]
Evers, B. Mark [1 ,2 ]
机构：
[1] Univ Texas Med Branch, Dept Surg, Galveston, TX USA
[2] Univ Texas Med Branch, Sealy Ctr Canc Cell Biol, Galveston, TX USA
来源：
ANTICANCER RESEARCH | 2009年 / 29卷 / 07期
基金：
美国国家卫生研究院;
关键词：
Inflammation; toll-like receptors; Akt; colon cancer; INFLAMMATORY-BOWEL-DISEASE; PROMOTES TUMOR-GROWTH; NF-KAPPA-B; COLORECTAL-CANCER; PHOSPHOINOSITIDE; 3-KINASES; HOMEOSTASIS; PROGRESSION; APOPTOSIS; PATHWAY;
D O I：
暂无
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
Background: Toll-like receptors (TLRs) are involved in innate immunity. Overexpression of TLRs has been implicated in various types of cancer including colorectal cancer (CRC). The phosphatidylinositol-3'-kinase (PI3K)/Akt signaling pathway is involved in CRC growth and progression. In this study, we determined whether TLR4 signaling and PI3K/Akt pathway activation occur in CRCs. Materials and Methods: Human CRCs and adjacent mucosa were evaluated for TLR4 expression. CRC cell lines were treated with lipopolysaccharide (LPS), endogenous TLR4 ligand, to assess Akt phosphorylation. Results: Human CRCs overexpressed TLR4 compared to matched normal mucosa. Additionally, TLR4 was expressed in CRC cells and LPS treatment increased Akt phosphorylation of TLR4-positive CRCs in a time-dependent manner. Conclusion: Our results identify TLR4 expression in human CRCs and activation of PI3K with LPS treatment. These findings suggest possible treatment strategies targeting TLR4 in CRC.
引用
收藏
页码：2473 / 2478
页数：6
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