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• W2054683516 abstract "Background Inflammation plays a multifaceted role in cancer progression, and NF-κB is one of the key factors connecting inflammation with cancer progression. We have shown that lipopolysaccharide (LPS) promotes NF-κB activation in colon cancer cells and pancreatic cancer cells. However, it is unclear why inflammatory stimuli can induce NF-κB activation in cancer cells. Methods We used two human pancreatic cancer cells, Panc-1 and AsPC-1, as target cells. LPS was used as an inflammatory stimulus. To confirm the participation of TLR4/NF-κB signaling pathway, we used three different NF-κB inhibitors (PDTC, IκBα mutant, and NF-κB decoy ODN) and siRNAs (against TLR4, MyD88, and MMP-9). Effect of LPS on pancreatic cancer cell invasive ability was determined by Matrigel invasion assay. Results LPS increased the invasive ability of pancreatic cancer cells, while blockade of NF-κB pathway decreased the LPS-dependent increased invasive ability. Blockade of TLR4 or MyD88 by siRNA also decreased the LPS-dependent increased invasive ability. Conclusion These results suggest that TLR/MyD88/NF-κB signaling pathway plays a significant role in connecting inflammation and cancer invasion and progression. J. Surg. Oncol. 2009;100:725–731. © 2009 Wiley-Liss, Inc." @default.
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• W2054683516 date "2009-08-31" @default.
• W2054683516 modified "2023-09-30" @default.
• W2054683516 title "Lipopolysaccharide (LPS) increases the invasive ability of pancreatic cancer cells through the TLR4/MyD88 signaling pathway" @default.
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• W2054683516 doi "https://doi.org/10.1002/jso.21392" @default.
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