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
The tumor promoting roles of long noncoding RNA (lncRNA) MALAT1 have been revealed in various cancers; however, its roles in esophageal squamous cell carcinoma (ESCC) have not previously been disclosed. In this study, we found that MALAT1 expression was remarkably increased in ESCC cells compared to normal human esophageal epithelial cells. In addition, knockdown of MALAT1 attenuated the stemness of ESCC cells, as evidenced by a decrease in spheroid formation capacity, stemness marker expression and aldehyde dehydrogenase 1 activity. Moreover, MALAT1 knockdown decreased the migration ability of ESCC cells. Notably, knockdown of MALAT1 enhanced the radiosensitivity and chemosensitivity of ESCC cells. We also established that MALAT1 binds directly to Yes-associated protein (YAP), thereby enhancing YAP protein expression and increasing YAP transcriptional activity. Overexpression of YAP partially rescued the effect of MALAT1 knockdown on stemness and radiosensitivity of ESCC cells. Overall, this study has identified that a novel MALAT1-YAP axis promotes the stemness of ESCC cells, and thus could be a potential target for treatment of ESCC.
Download full-text PDF |
Source |
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6668371 | PMC |
http://dx.doi.org/10.1002/2211-5463.12676 | DOI Listing |
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