Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2010-11-12
pubmed:abstractText
Increasing evidence suggests that thiazolidinediones (TZDs) could have a therapeutic potential for patients with cancers. Here, the evidence on the mechanisms by which TZDs could contribute to different steps of cancer biology in the digestive system is summarized. According to studies, TZDs induce anti-cancer actions through 3 main pathways: (1) cell growth arrest, (2) induction of apoptosis, and (3) inhibition of cell invasion. Cell growth arrest is induced by an increased level of p27(Kip1). p27(Kip1) accumulation results from the inhibition of the ubiquitin-proteasome system and/or inhibition of MEK-ERK signaling. TZDs induce apoptosis through increased levels of apoptotic molecules, such as p53 and PTEN and/or decreased level of anti-apoptotic molecules, such as Bcl-2 and survivin. Inhibition of MEK-ERK signaling-mediated up-regulation of E-cadherin and claudin-4, and/or decreased expression of matrix metalloproteinases (MMPs) such as MMP-2 and MMP-9, play a role in the TZD-induced inhibition of cancer cell invasion. Thus, TZDs are capable of inducing anti-tumor action in a variety of ways in gastrointestinal cancers.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1435-5922
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
45
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1097-102
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Mechanisms by which thiazolidinediones induce anti-cancer effects in cancers in digestive organs.
pubmed:affiliation
Department of General Medicine, Asahikawa Medical University, Asahikawa, Hokkaido, Japan. okumurat@asahikawa-med.ac.jp
pubmed:publicationType
Journal Article, Review