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
Previous reports revealed that a significant decrease of miR-34a in oral cancer. But the role of miR-34a in oral cancer needs further research. In the present study, we will investigate the effect of miR-34a on oral cancer cell phenotypes. First, it was verified that miR-34a expression was lower in oral cancer tissues compared with their normal controls, so did the oral cancer cells. Next, it was showed that miR-34a overexpression in oral cancer cells could inhibit cell proliferation, G1 phase arrest, metastasis and epithelial mesenchymal transition. It was predicted that interleukin-6-receptor (IL6R) was a potential target gene of miR-34a by bioinformatics analysis and identified by luciferase assay. It was further showed that miR-34a inhibited oral cancer progression via IL6R. Collectively, our findings suggested that miR-34a may function as a tumor suppressor in oral cancer by targeting IL6R.
Download full-text PDF |
Source |
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4396206 | PMC |
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