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
The role of miR-339 in human gastric cancer (GC) remains unclear. Here, we found that miR-339 is remarkably decreased in primary GC tissues. Overexpression of miR-339 in GC cells significantly suppressed proliferation, migration, invasion, and tumorigenicity. Furthermore, NOVA1 was confirmed as a target of miR-339. Restoration of NOVA1 in miR-339-overexpressing GC cells partially impaired the inhibitory effects of miR-339. More importantly, epigenetic modification may be involved in the modulation of miR-339 expression. These findings uncover a novel role for miR-339 in gastric carcinogenesis, and restoration of miR-339 could be considered as a potential therapeutic strategy for GC treatment.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1016/j.febslet.2015.09.009 | DOI Listing |
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