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
miR-122 may function as a novel tumor suppressor. Expression of miR-122 could suppress the proliferation of multi-kinds of human cancer cell lines. In this work, expression of miR-122 via adenoviral vector in non-small-cell lung cancer (NSCLC) cells reduces the number of invasion and migration cells. miR-122 attenuates the epithelial-mesenchymal transition process, which mediates cancer cells metastasis in NSCLC cells A549 and H460. The mechanisms data reveals that miR-122 would disrupt the epithelial-mesenchymal transition process by downregulating PI3K/AKT activation via reducing endogenous expression of insulin-like growth factor 1 receptor. These data highlight the detailed roles and potential application of miR-122 in NSCLC cells.
Download full-text PDF |
Source |
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4631421 | PMC |
http://dx.doi.org/10.2147/OTT.S91696 | DOI Listing |
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