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, IkBa 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.
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