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
Background: Aberrant miRNAs expression regulates the occurrence and progression of a variety of cancers, including oral squamous cell carcinoma (OSCC). This study aims to illustrate the potential effects of miR-454/nuclear receptor subfamily 3 group C member 2 (NR3C2) on the biological behaviors of OSCC cells.
Methods: GEO database was applied to detect and analyze the expression of miR-545 and NR3C2 in OSCC tissues. Two OSCC cell lines including CAL27 and Tca-83 were utilized to determine the function of miR-454/NR3C2 on OSCC cells biological behaviors. miR-454 and NR3C2 expressions were regulated by miR-454 mimic/inhibitor and pcDNA3.1-NR3C2/si-NR3C2, respectively. Cells biological behaviors were evaluated by cell proliferation, colony formation, and transwell assays.
Results: The data collected from GEO database indicated that miR-454 expression was upregulated in OSCC tissues; however, the expression of NR3C2 assumed a downward trend. In vitro experiments, the expression trend of miR-454 in OSCC cell lines was consistent with that of the trend in tissues, and the OSCC cells growth and movement abilities significantly decreased after miR-454 depletion. Through co-transfection experiments, we explored that the abilities of OSCC cell proliferation, colony formation, invasion, and migration obviously reduced after miR-454 depletion, but these phenomena were mitigated to some extent after NR3C2 silencing.
Conclusion: The study illustrates that miR-454 acts as an active regulator to facilitate OSCC cells growth, colony formation, invasion, and migration by targeting NR3C2, which may afford a novel perspective and possibility for the targeted treatment of OSCC.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1111/jop.13015 | DOI Listing |
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