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: 1034
Function: getPubMedXML
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3152
Function: GetPubMedArticleOutput_2016
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
The therapeutics of lung cancer (LC) is unsatisfactory. The pathogenesis of LC remains unclear. Protease-activated receptors (PAR) are involved in the immunoregulation. The present study aims to investigate the activation of PAR2 in regulation of the expression of EGFR and apoptosis of LC cells. The results showed that exposure to tryptase increased EGFR expression in A549 cells and suppressed the cell apoptosis. Tryptase also decreased the expression of Bax and increased Bcl-xL levels in A549 cells. We conclude that activation of PAR2 by tryptase can decrease the ratio of Bax/Bcl-xL and reduce the LC cell line, A549 cells, and apoptosis.
Download full-text PDF |
Source |
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http://dx.doi.org/10.3109/07357907.2013.845674 | DOI Listing |
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