In our study, TLR4 knockdown in vitro lead to TLR4-related inflam

In our study, TLR4 knockdown in vitro lead to TLR4-related inflammatory cytokines being markedly depressed and so it could weaken the ability to the resistance of MDA-MB-231 to CTL and NKC attack and facilitate evasion from immune surveillance. This occurrence in vitro

may indicate us that TLR4 knockdown in vivo could inhibit the growth and promote the death Ro 61-8048 research buy of breast tumors. Conclusions TLR4-mediated cancer growth appears to be an important factor in tumor progression. The use of systemically delivered TLR4-siRNA may provide a novel approach to preventing cancer progression and survival. TLR4AsiRNA directed targeting of TLR4 is a promising candidate for molecular therapy of breast cancer. Acknowledgements This work was supported by Professor Dongxu Liu of Hubei University. References 1. Medzhitov R, Preston-Hurlburt P, Janeway CA Jr: A human homologue of the Drosophila Toll protein signals activation of adaptive immunity. Nature 1997,388(6640):394–397.PubMedCrossRef 2. Takeda K, Kaisho T, Akira S: Toll-like receptors. Annu Rev Immunol 2003, 21:335–376.PubMedCrossRef 3. Medzhitov PSI-7977 datasheet R, Janeway CA Jr: Decoding the patterns of self and nonself by the innate immune system. Science 2002,296(5566):298–300.PubMedCrossRef

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