Research Papers:

Adenomatous polyposis coli genotype-dependent toll-like receptor 4 activity in colon cancer

Feng Wen, Yongmei Liu, Wei Wang, Meng Li, Fuchun Guo, Yaxiong Sang, Qing Qin, Yongsheng Wang and Qiu Li _

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Oncotarget. 2016; 7:7761-7772. https://doi.org/10.18632/oncotarget.6844

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Feng Wen1,*, Yongmei Liu1,*, Wei Wang2, Meng Li2, Fuchun Guo1, Yaxiong Sang2, Qing Qin1, Yongsheng Wang1, Qiu Li1

1The Department of Medical Oncology, Cancer Center, State Key Laboratory of Biotherapy/Collaborative Innovation Center for Biotherapy, West China Hospital, University of Sichuan, Sichuan, China

2State Key Laboratory of Biotherapy and Cancer Center/Collaborative Innovation Center for Biotherapy, West China Hospital, University of Sichuan, Sichuan, China

*These authors have contributed equally to this work

Correspondence to:

Yongsheng Wang, e-mail: [email protected]

Qiu Li, e-mail: [email protected]

Keywords: adenomatous polyposis coli, NF-κB, β-catenin, colon cancer

Received: July 30, 2015     Accepted: January 01, 2016     Published: January 8, 2016


Toll-like receptors (TLRs)/NF-κB activation stimulated by lipopolysaccharide (LPS) was associated with diverse biological response in colon cancer, but the underlying mechanism was largely unknown. In the current study, we reported cell proliferation was elevated in adenomatous polyposis coli (APC) mutated- and APC knockdown cell lines, while the proliferation was inhibited in APC wild-type cell lines. Besides, in vivo experiments showed that LPS promoted APC knockdown tumor growth while inhibited proliferation of APC wild type. Further study confirmed that activation of TLRs/NF-κB signaling pathway by LPS cross regulated with APC/GSK-3β/β-catenin pathway, which were depend on APC status of cell lines. Taken together, APC genotypes play a key role in LPS induced different colon cancer biological response by cross-regulating β-catenin and NF-κB, which may provide a novel strategy for carcinogenesis prevention.

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