Severity: Warning
Message: file_get_contents(https://...@gmail.com&api_key=61f08fa0b96a73de8c900d749fcb997acc09&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 197
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 197
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 271
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 1075
Function: getPubMedXML
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3195
Function: GetPubMedArticleOutput_2016
File: /var/www/html/application/controllers/Detail.php
Line: 597
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 511
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 317
Function: require_once
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Glioblastoma is a highly malignant brain tumor, characterized by the poor prognosis and high recurrence rates. Despite therapeutic strategies including surgery, radiotherapy and chemotherapy, the median survival of patients is only 14.6 months. MicroRNAs (miRNAs) have been considered as a novel type of gene regulator. Previous studies have demonstrated that the expression of miRNA‑34a (miR‑34a) is significantly associated with the grade and prognosis of glioma. However, the exact function of miR‑34a on glioma progression and underlying mechanisms remain to be elucidated. The present study investigated the function of miR‑34a in U87 human glioma cells by exogenously transfecting cells with an miR‑34a mimic. Overexpression of miR‑34a inhibited proliferation, and induced apoptosis of U87 cells. The current study also demonstrated that B‑cell lymphoma 2 (Bcl‑2) was the target gene of miR‑34a, as demonstrated by luciferase assays. Furthermore, restoring the expression of Bcl‑2 was indicated to partially block the miR‑34a‑induced apoptosis. Thus, data from the present study identified miR‑34a as a tumor suppressor in glioma by, at least partially, targeting Bcl‑2. This may provide future novel diagnostic and therapeutic strategies for human glioma.
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http://dx.doi.org/10.3892/mmr.2016.5255 | DOI Listing |