Lipopolysaccharide (LPS) increases the invasive ability of pancreatic cancer cells through the TLR4/MyD88 signaling pathway

Mio Ikebe, Yoshiki Kitaura, Masafumi Nakamura, Haruo Tanaka, Akio Yamasaki, Shuntaro Nagai, Junji Wada, Kosuke Yanai, Kenichiro Koga, Norihiro Sato, Makoto Kubo, Masao Tanaka, Hideya Onishi, Mitsuo Katano

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86 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)725-731
Number of pages7
JournalJournal of Surgical Oncology
Issue number8
Publication statusPublished - Dec 15 2009


All Science Journal Classification (ASJC) codes

  • Surgery
  • Oncology

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