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
Hepatocellular carcinoma (HCC) is a primary malignancy of the liver. It has been reported that microRNAs (miRs) play important roles in the progression and development of HCC. The expression of miR-490-3p has been shown to be downregulated in HCC tissues. Therefore, the present study aimed to investigate the effects of miR-490-3p on HCC cells and the underlying mechanism. Cell Counting Kit-8, flow cytometry, and Transwell migration and invasion assays were performed to determine the viability, apoptosis, migration and invasion of HCC cells, respectively. Furthermore, a luciferase activity assay was used to verify the association between miR-490-3p and its predicted target tropomodulin 3 (TMOD3). In addition, the protein levels of Bax, Bcl-2, cleaved caspase-3, TMOD3, phosphorylated (p)-p38 and p-ERK in HCC cells were detected using western blot analysis. The results demonstrated that the overexpression of miR-490-3p via transfection with miR-490-3p mimics significantly inhibited the proliferation of Huh-7 and HEP 3B2.1-7 cells. In addition, overexpression of miR-490-3p markedly suppressed the migration and invasion abilities of Huh-7 cells. miR-490-3p mimics significantly induced liver cancer cell apoptosis via upregulating Bax and cleaved caspase-3 and downregulating anti-apoptotic protein Bcl-2. Additionally, a luciferase activity assay indicated that TMOD3 is a downstream target gene of miR-490-3p. The protein levels of TMOD3, p-p38 and p-ERK were significantly downregulated in Huh-7 cells following transfection with miR-490-3p mimics, and the overexpression of TMOD3 attenuated these effects. In conclusion, the aforementioned results suggest that the overexpression of miR-490-3p inhibited the proliferation and invasion of HCC cells by targeting TMOD3. Therefore, the miR-490-3p/TMOD3 axis may be a potent target for the treatment of HCC.
Download full-text PDF |
Source |
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7439154 | PMC |
http://dx.doi.org/10.3892/ol.2020.11956 | DOI Listing |
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