Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2003-4-9
pubmed:abstractText
Metastasis is largely an unsuccessful process, because the majority of disseminating tumor cells demise shortly after reaching distant organs. Therefore, survival is essential for disseminating tumor cells to establish metastases. During metastasis, interaction between tumor and host cells leads to the production of nitric oxide (NO). An increasing amount of evidence suggests that NO regulates tumor-cell survival and influences cancer metastasis. The ultimate effect of NO on tumor-cell survival is dictated by multiple factors, including the levels of NO production and genetic and epigenetic makeup of the tumor cells. Also, expression of inducible nitric oxide synthase (NOS) II has the potential to produce NO at a toxic level and tumor-cell death via apoptosis. Yet, impaired NOS II expression during tumor progression may lead to decreased NO production, which may be insufficient to produce significant cytotoxic effects, and the subsequent low level of NO production may cause induction of NO resistance, and the NO-resistant tumor cells may usurp NO to undergo progression. Thus, restoration of NOS II expression and reversal of NO resistance may prevent tumor growth and metastasis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0891-5849
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
34
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
969-86
pubmed:dateRevised
2011-10-27
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Contribution of nitric oxide-mediated apoptosis to cancer metastasis inefficiency.
pubmed:affiliation
Gastrointestinal Medical Oncology, The University of Texas M D Anderson Cancer Center, Houston, TX 77030, USA. kepxie@mail.mdanderson.org
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, Non-U.S. Gov't