Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.ccr.2012.08.010
Title: STAT3-Driven Upregulation of TLR2 Promotes Gastric Tumorigenesis Independent of Tumor Inflammation
Authors: Tye, H.
Kennedy, C.
Najdovska, M.
McLeod, L.
McCormack, W.
Hughes, N.
Dev, A.
Sievert, W.
Ooi, C. 
Ishikawa, T.-O.
Oshima, H.
Bhathal, P.
Parker, A.
Oshima, M.
Tan, P. 
Jenkins, B.
Issue Date: 16-Oct-2012
Citation: Tye, H., Kennedy, C., Najdovska, M., McLeod, L., McCormack, W., Hughes, N., Dev, A., Sievert, W., Ooi, C., Ishikawa, T.-O., Oshima, H., Bhathal, P., Parker, A., Oshima, M., Tan, P., Jenkins, B. (2012-10-16). STAT3-Driven Upregulation of TLR2 Promotes Gastric Tumorigenesis Independent of Tumor Inflammation. Cancer Cell 22 (4) : 466-478. ScholarBank@NUS Repository. https://doi.org/10.1016/j.ccr.2012.08.010
Abstract: Gastric cancer (GC) is associated with chronic inflammation; however, the molecular mechanisms promoting tumorigenesis remain ill defined. Using a GC mouse model driven by hyperactivation of the signal transducer and activator of transcription (STAT)3 oncogene, we show that STAT3 directly upregulates the epithelial expression of the inflammatory mediator Toll-like receptor (TLR)2 in gastric tumors. Genetic and therapeutic targeting of TLR2 inhibited gastric tumorigenesis, but not inflammation, characterized by reduced proliferation and increased apoptosis of the gastric epithelium. Increased STAT3 pathway activation and TLR2 expression were also associated with poor GC patient survival. Collectively, our data reveal an unexpected role for TLR2 in the oncogenic function of STAT3 that may represent a therapeutic target in GC. © 2012 Elsevier Inc.
Source Title: Cancer Cell
URI: http://scholarbank.nus.edu.sg/handle/10635/110635
ISSN: 15356108
DOI: 10.1016/j.ccr.2012.08.010
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