Severity: Warning
Message: file_get_contents(https://...@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b4908&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 176
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 176
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 250
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3122
Function: getPubMedXML
File: /var/www/html/application/controllers/Detail.php
Line: 575
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 489
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
Reactive oxygen species (ROS) are important contributors to tumor cell invasion. ROS enhanced by reactive oxygen species modulator 1 (Romo1) expression has been reported to increase invasive potential and constitutive activation of nuclear factor-κB (NF-κB) in hepatocellular carcinoma (HCC). Therefore, we investigated whether constitutive NF-κB activation due to Romo1 expression is associated with breast cancer tumor cell invasion. In this study, we show that oxidative stress-induced invasion is mediated by Romo1 expression. The Romo1-induced increase of invasive activity was blocked by an inhibitor of κB kinase (IKK). These results demonstrate that tumor cell invasion in response to oxidative stress is associated with Romo1 expression and the NF-κB signaling pathway. Romo1 is therefore a promising therapeutic target for diseases characterized by NF-κB deregulation.
Download full-text PDF |
Source |
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http://dx.doi.org/10.3892/ijo.2015.2889 | DOI Listing |
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