PMID- 25548469
OWN - NLM
STAT- MEDLINE
DCOM- 20150910
LR  - 20220409
IS  - 2219-2840 (Electronic)
IS  - 1007-9327 (Print)
IS  - 1007-9327 (Linking)
VI  - 20
IP  - 47
DP  - 2014 Dec 21
TI  - Toll-like receptor signaling in colorectal cancer: carcinogenesis to cancer 
      therapy.
PG  - 17699-708
LID - 10.3748/wjg.v20.i47.17699 [doi]
AB  - Toll-like receptors (TLRs) are germ line encoded innate immune sensors that 
      recognize conserved microbial structures and host alarmins, and signal expression 
      of major histocompatibility complex proteins, costimulatory molecules, and 
      inflammatory mediators by macrophages, neutrophils, dendritic cells, and other 
      cell types. These protein receptors are characterized by their ability to respond 
      to invading pathogens promptly by recognizing particular TLR ligands, including 
      flagellin and lipopolysaccharide of bacteria, nucleic acids derived from viruses, 
      and zymosan of fungi. There are 2 major TLR pathways; one is mediated by myeloid 
      differentiation factor 88 (MYD88) adaptor proteins, and the other is independent 
      of MYD88. The MYD88-dependent pathway involves early-phase activation of nuclear 
      factor of kappa light polypeptide gene enhancer in B-cells 1 (NF-kappaB1) and all the 
      TLRs, except TLR3, have been shown to activate this pathway. TLR3 and TLR4 act 
      via MYD88-independent pathways with delayed activation of NF-kappaB signaling. TLRs 
      play a vital role in activating immune responses. TLRs have been shown to mediate 
      inflammatory responses and maintain epithelial barrier homeostasis, and are 
      highly likely to be involved in the activation of a number of pathways following 
      cancer therapy. Colorectal cancer (CRC) is one of the most common cancers, and 
      accounts for almost half a million deaths annually worldwide. Inflammation is 
      considered a risk factor for many common malignancies including cancers of the 
      colorectum. The key molecules involved in inflammation-driven carcinogenesis 
      include TLRs. As sensors of cell death and tissue remodeling, TLRs may have a 
      universal role in cancer; stimulation of TLRs to activate the innate immune 
      system has been a legitimate therapeutic strategy for some years. TLRs 3/4/7/8/9 
      are all validated targets for cancer therapy, and a number of companies are 
      developing agonists and vaccine adjuvants. On the other hand, antagonists may 
      favor inhibition of signaling responsible for autoimmune responses. In this 
      paper, we review TLR signaling in CRC from carcinogenesis to cancer therapy.
FAU - Li, Ting-Ting
AU  - Li TT
AD  - Ting-Ting Li, Department of Geriatric Gastroenterology, Chinese PLA General 
      Hospital, Beijing 100853, China.
FAU - Ogino, Shuji
AU  - Ogino S
AD  - Ting-Ting Li, Department of Geriatric Gastroenterology, Chinese PLA General 
      Hospital, Beijing 100853, China.
FAU - Qian, Zhi Rong
AU  - Qian ZR
AD  - Ting-Ting Li, Department of Geriatric Gastroenterology, Chinese PLA General 
      Hospital, Beijing 100853, China.
LA  - eng
GR  - P01 CA087969/CA/NCI NIH HHS/United States
GR  - P01 CA055075/CA/NCI NIH HHS/United States
GR  - R01 CA151993/CA/NCI NIH HHS/United States
GR  - R01 CA137178/CA/NCI NIH HHS/United States
GR  - P01 CA87969/CA/NCI NIH HHS/United States
GR  - P01 CA55075/CA/NCI NIH HHS/United States
GR  - UM1 CA167552/CA/NCI NIH HHS/United States
GR  - P50 CA127003/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United States
TA  - World J Gastroenterol
JT  - World journal of gastroenterology
JID - 100883448
RN  - 0 (Antineoplastic Agents)
RN  - 0 (Cancer Vaccines)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Toll-Like Receptors)
SB  - IM
MH  - Animals
MH  - Antineoplastic Agents/therapeutic use
MH  - Cancer Vaccines/therapeutic use
MH  - Cell Transformation, Neoplastic/immunology/*metabolism/pathology
MH  - Colorectal Neoplasms/immunology/*metabolism/pathology/*therapy
MH  - Humans
MH  - Inflammation Mediators/immunology/*metabolism
MH  - Molecular Targeted Therapy
MH  - *Signal Transduction/drug effects
MH  - Toll-Like Receptors/drug effects/immunology/*metabolism
PMC - PMC4273121
OTO - NOTNLM
OT  - Cancer therapy
OT  - Carcinogenesis
OT  - Colorectal cancer
OT  - Prognosis
OT  - Toll-like receptor
EDAT- 2014/12/31 06:00
MHDA- 2015/09/12 06:00
PMCR- 2014/12/21
CRDT- 2014/12/31 06:00
PHST- 2014/05/28 00:00 [received]
PHST- 2014/08/27 00:00 [revised]
PHST- 2014/11/18 00:00 [accepted]
PHST- 2014/12/31 06:00 [entrez]
PHST- 2014/12/31 06:00 [pubmed]
PHST- 2015/09/12 06:00 [medline]
PHST- 2014/12/21 00:00 [pmc-release]
AID - 10.3748/wjg.v20.i47.17699 [doi]
PST - ppublish
SO  - World J Gastroenterol. 2014 Dec 21;20(47):17699-708. doi: 
      10.3748/wjg.v20.i47.17699.