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
Aim: We aim to investigate the functions of PXN in cervical cancer.
Materials & Methods: PXN protein was investigated by immunohistochemistry in a panel of cervical cancer. A series of in vitro and in vivo assays were used to explore the efficacy of PXN.
Results: PXN was significantly upregulated in cervical cancer, which associated with tumor stage, poor differentiation, lymphovascular space invasion and lymphatic metastasis. Knockdown of PXN notably impaired cellular growth and colony formation by suppressing Bcl-2 and inducing marked apoptosis. Moreover, PXN led to resistance to radiation, and downregulation of PXN resensitized C33A cells to radiation.
Conclusion: PXN was frequently upregulated and acted as an oncogene via regulating Bcl-2 in cervical cancer, which supports PXN as a potent therapeutic target.
Download full-text PDF |
Source |
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http://dx.doi.org/10.2217/fon-2017-0474 | DOI Listing |
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