TLR4/PKC‐mediated tight junction modulation: A clinical marker of chemotherapy‐induced gut toxicity?

Chemotherapy‐induced gut toxicity is a major clinical and economic burden to oncology practice. The mechanisms responsible for its development are ill defined, hampering the development of therapeutic interventions. In light of newly published research foci and clinical practice guidelines in suppor...

Full description

Saved in:
Bibliographic Details
Published in:International journal of cancer 2014-12, Vol.135 (11), p.2483-2492
Main Authors: Wardill, Hannah R., Gibson, Rachel J., Logan, Richard M., Bowen, Joanne M.
Format: Article
Language:English
Subjects:
Antineoplastic Agents - adverse effects
Biomarkers - metabolism
Cancer
Chemotherapy
Digestive system
Disruption
Gastrointestinal Diseases - chemically induced
Gastrointestinal Diseases - metabolism
Gastrointestinal tract
Humans
Immune system
Intestine
Kinases
Medical research
mucositis
Oncology
Protein kinase C
Protein Kinase C - metabolism
Signal Transduction
Therapeutic applications
Tight junctions
Tight Junctions - metabolism
TLR4 protein
Toll-Like Receptor 4 - metabolism
Toll-like receptors
toll‐like receptor 4
Toxicity
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Chemotherapy‐induced gut toxicity is a major clinical and economic burden to oncology practice. The mechanisms responsible for its development are ill defined, hampering the development of therapeutic interventions. In light of newly published research foci and clinical practice guidelines in supportive care in cancer, there has been renewed interest in the role tight junctions play in the pathobiology of chemotherapy‐induced gut toxicity. Several preclinical studies have identified molecular defects in intestinal tight junctions following chemotherapy. Despite these findings, the mechanisms responsible for chemotherapy‐induced tight junction disruption remain unclear. Recent research has highlighted roles for toll‐like receptor 4 and protein kinase C signalling in the regulation of tight junctions. This critical review therefore aims to provide evidence linking toll‐like receptor 4 expression, protein kinase C activation and tight junction disruption and their relationship to clinical toxicity.
ISSN:0020-7136
1097-0215
DOI:10.1002/ijc.28656