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
Cancer stem cells (CSCs) have been suggested to be responsible for tumor re-growth and relapse. Physiological and morphological knowledge of CSCs may be essential for the development of new therapeutic strategies targeting cancer development, progression, and recurrence. Current research is focused on a deeper understanding of CSCs metabolic profiles, taking into consideration their energy demands. Energy metabolism and mitochondrial function are important factors operating on stemness maintenance and cell fate specification. Due to the role of mitochondria as central hubs in the overall cell metabolism and death and survival pathways, research on their physiology in CSCs is of paramount importance to decipher mechanisms underlying their therapy-resistant phenotype. In this review, we focus on CSCs mitochondrial biology and mitochondria-related signaling pathways that contribute to CSCs survival and maintenance, thereby representing possible therapeutic targets.
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Source |
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http://dx.doi.org/10.1016/j.semcancer.2017.06.012 | DOI Listing |
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