Inflammation, cancer and chemoresistance: Taking advantage of the toll-like receptor signaling pathway

被引:141
作者
Chen, Rui
Alvero, Ayesha B.
Silasi, Dan-Arin
Mor, Gil
机构
[1] Yale Univ, Sch Med, Dept Obstet Gynecol & Reprod Sci, Reprod Immunol Unit, New Haven, CT 06520 USA
[2] Yale Univ, Dept Mol Cellular & Dev Biol, New Haven, CT 06520 USA
关键词
chemokines; chemoresistance; epithelial ovarian cancer; MyD88; paclitaxel; Toll-like receptor;
D O I
10.1111/j.1600-0897.2006.00441.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The association between chronic inflammation and cancer has long been observed. Furthermore, NF-kappa B activation and the subsequent production of cytokines, chemokines, growth factors, and antiapoptotic proteins has been found to be involved in cancer progression and chemoresistance. However, the signals inducing NF-kappa B in cancer cells are still not well understood. Here, we reviewed the association between chronic inflammation and cancer, the role of NF-kappa B and its inhibitors as potential anticancer drugs, and Toll-like receptors as possible signal initiators for NF-kappa B activation and inflammation-induced carcinogenesis and chemoresistance. Furthermore, we propose that, the stimulation of Toll-like receptors by microbial components and/or endogenous ligands may represent the initial signal promoting a proinflammatory environment that will enhance tumor growth and chemoresistance.
引用
收藏
页码:93 / 107
页数:15
相关论文
共 109 条
[51]   Chromatin-IgG complexes activate B cells by dual engagement of IgM and Toll-like receptors [J].
Leadbetter, EA ;
Rifkin, IR ;
Hohlbaum, AM ;
Beaudette, BC ;
Shlomchik, MJ ;
Marshak-Rothstein, A .
NATURE, 2002, 416 (6881) :603-607
[52]   Regulation of interleukin-6 gene expression by pro-inflammatory cytokines in a colon cancer cell line [J].
Legrand-Poels, S ;
Schoonbroodt, S ;
Piette, J .
BIOCHEMICAL JOURNAL, 2000, 349 :765-773
[53]   The dorsoventral regulatory gene cassette spatzle/Toll/cactus controls the potent antifungal response in Drosophila adults [J].
Lemaitre, B ;
Nicolas, E ;
Michaut, L ;
Reichhart, JM ;
Hoffmann, JA .
CELL, 1996, 86 (06) :973-983
[54]   Distinct role of macrophages in different tumor microenvironments [J].
Lewis, CE ;
Pollard, JW .
CANCER RESEARCH, 2006, 66 (02) :605-612
[55]   Inflammation-associated cancer:: NF-κB is the lynchpin [J].
Li, QT ;
Withoff, S ;
Verma, IM .
TRENDS IN IMMUNOLOGY, 2005, 26 (06) :318-325
[56]   High-mobility group box 1 protein (HMGB): Nuclear weapon in the immune arsenal [J].
Lotze, MT ;
Tracey, KJ .
NATURE REVIEWS IMMUNOLOGY, 2005, 5 (04) :331-342
[57]   Inhibition of NF-κB in cancer cells converts inflammation-induced tumor growth mediated by TNFα to TRAIL-mediated tumor regression [J].
Luo, JL ;
Maeda, S ;
Hsu, LC ;
Yagita, H ;
Karin, M .
CANCER CELL, 2004, 6 (03) :297-305
[58]   Inhibition of NFκB increases the efficacy of cisplatin in in vitro and in vivo ovarian cancer models [J].
Mabuchi, S ;
Ohmichi, M ;
Nishio, Y ;
Hayaska, T ;
Kimura, A ;
Ohta, T ;
Saito, M ;
Kawagoe, J ;
Takahashi, K ;
Yada-Hashimoto, N ;
Sakata, M ;
Motoyama, T ;
Kurachi, H ;
Tasaka, K ;
Murata, Y .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (22) :23477-23485
[59]   Cancer - Inflammation by remote control [J].
Mantovani, A .
NATURE, 2005, 435 (7043) :752-753
[60]   Cancer research - Inflammation and cancer: The link grows stronger [J].
Marx, J .
SCIENCE, 2004, 306 (5698) :966-968