Linked Life Data

21540248

Source:http://linkedlifedata.com/resource/pubmed/id/21540248

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2011-5-9
pubmed:abstractText
Arsenic trioxide (As(2)O(3)) has been shown to inhibit invasion/migration in cancer cells. However, the underlying mechanism is poorly understood. To identify the role of As(2)O(3) in regulating invasion/migration activity in human gastric cancer SGC-7901 cells, the effects of As(2)O(3) on cell invasion/migration activity, the expression of cyclooxygenase-2 (Cox-2), prostaglandin E2 (PGE2), thromboxane B2 (TXB2), leukotriene B4 (LTB4), and matrix metalloproteinase-2 (MMP-2) and intracellular reactive oxygen species (ROS) were examined. Furthermore, N-acetyl-l-cysteine (NAC, a radical scavenger) and celecoxib (a Cox-2 inhibitor) were used to explore the molecular mechanism. The results demonstrated that As(2)O(3) (1 and 2 ?mol/L) inhibited invasion/migration activity in SGC-7901 cells at 24 h and suppressed the expression of Cox-2, PGE2 and MMP-2 (P < 0.05), whereas the same treatment had no significant effect on TXB2 and LTB4 expression. In contrast, intracellular ROS were increased (P < 0.05). Moreover, NAC eliminated the excessive ROS and restored the expression of Cox-2 and MMP-2 and invasion/migration activity in As(2)O(3)-treated cells (P < 0.05). These results suggest that ROS may be a critical factor in regulating the invasion/migration process. Moreover, celecoxib significantly decreased Cox-2, MMP-2 and PGE2 expression and inhibited invasion/migration activity in As(2)O(3)-treated cells (P < 0.05), indicating that As(2)O(3) inhibits invasion/migration by regulating the expression of Cox-2/PGE2/MMP-2. In conclusion, these results suggest that increased ROS play a critical role in inhibiting invasion/migration by suppressing the Cox-2/MMP-2 pathway in As(2)O(3)-treated SGC-7901 cells and regulating intracellular ROS levels may be a promising strategy in gastric cancer therapy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1535-3699
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
236
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
592-7
pubmed:meshHeading
pubmed-meshheading:21540248-Arsenicals, pubmed-meshheading:21540248-Cell Line, Tumor, pubmed-meshheading:21540248-Cell Movement, pubmed-meshheading:21540248-Cyclooxygenase 2, pubmed-meshheading:21540248-Dinoprostone, pubmed-meshheading:21540248-Enzyme Activation, pubmed-meshheading:21540248-Gene Expression Regulation, Enzymologic, pubmed-meshheading:21540248-Gene Expression Regulation, Neoplastic, pubmed-meshheading:21540248-Humans, pubmed-meshheading:21540248-Intracellular Space, pubmed-meshheading:21540248-Leukotriene B4, pubmed-meshheading:21540248-Matrix Metalloproteinase 2, pubmed-meshheading:21540248-Neoplasm Invasiveness, pubmed-meshheading:21540248-Oxides, pubmed-meshheading:21540248-Reactive Oxygen Species, pubmed-meshheading:21540248-Signal Transduction, pubmed-meshheading:21540248-Thromboxane B2
pubmed:year
2011
pubmed:articleTitle
Arsenic trioxide inhibits invasion/migration in SGC-7901 cells by activating the reactive oxygen species-dependent cyclooxygenase-2/matrix metalloproteinase-2 pathway.
pubmed:affiliation
Key Laboratory of Arid and Grassland Ecology, Ministry of Education/Arid Laboratory, School of Life Sciences, Lanzhou University, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't