| http://purl.uniprot.org/citations/32191537 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/32191537 | http://www.w3.org/2000/01/rdf-schema#comment | "Background: Hepatocellular carcinoma (HCC) has high morbidity and mortality, but current therapeutic methods cannot effectively improve patient's prognosis. FOXD3-AS1, a new identified long noncoding RNA, is dysregulated in several cancers and functions as a carcinogenic or tumor-suppressor factor. However, the function of FOXD3-AS1 in HCC has not been reported. Materials and Methods: Quantitative real time-polymerase chain reaction was applied to evaluate the expression of FOXD3-AS1 in HCC tissues and cell lines. miRDB and TargetScan websites were utilized to predict the interaction network of FOXD3-AS1 as a competing endogenous RNA. The interaction was confirmed by luciferase reporter assay and RNA binding protein immunoprecipitation (RIP) assay. The effect of FOXD3-AS1 on HCC cells (Huh6) were measured by cell counting kit (CCK)-8, BrdU cell proliferation assay, Transwell invasion assay, and wound healing assay. Results: FOXD3-AS1 was overexpressed in HCC, and HCC patients with the high level of FOXD3-AS1 had a poor prognosis. In addition, FOXD3-AS1 knockdown considerably inhibited the proliferation, migration, and invasion of Huh6 cells. Besides, FOXD3-AS1 functioned as a sponge of miR-335, and RICTOR was a direct target gene of miR-335. Furthermore, FOXD3-AS1 could enhance the level of RICTOR through sponging miR-335. Moreover, the knockdown of FOXD3-AS1 could competitively bind with miR-335 to suppress RICTOR expression, thereby inhibiting the growth of Huh6 cells through the deactivation of AKT signaling pathway. Conclusions: FOXD3-AS1 is crucial for the tumorigenesis and progression of HCC. The interaction among FOXD3-AS1, miR-335, and RICTOR provides a novel insight for understanding the molecular mechanism of HCC, and FOXD3-AS1, miR-335, and RICTOR can be regarded as the potential targets for HCC treatment."xsd:string |
| http://purl.uniprot.org/citations/32191537 | http://purl.org/dc/terms/identifier | "doi:10.1089/cbr.2019.3335"xsd:string |
| http://purl.uniprot.org/citations/32191537 | http://purl.uniprot.org/core/author | "Liu C."xsd:string |
| http://purl.uniprot.org/citations/32191537 | http://purl.uniprot.org/core/author | "Zhang X."xsd:string |
| http://purl.uniprot.org/citations/32191537 | http://purl.uniprot.org/core/author | "Zhang R."xsd:string |
| http://purl.uniprot.org/citations/32191537 | http://purl.uniprot.org/core/author | "Zhu X."xsd:string |
| http://purl.uniprot.org/citations/32191537 | http://purl.uniprot.org/core/author | "Zhu L."xsd:string |
| http://purl.uniprot.org/citations/32191537 | http://purl.uniprot.org/core/author | "Zhao J."xsd:string |
| http://purl.uniprot.org/citations/32191537 | http://purl.uniprot.org/core/author | "Zhang M."xsd:string |
| http://purl.uniprot.org/citations/32191537 | http://purl.uniprot.org/core/author | "Yan M."xsd:string |
| http://purl.uniprot.org/citations/32191537 | http://purl.uniprot.org/core/date | "2020"xsd:gYear |
| http://purl.uniprot.org/citations/32191537 | http://purl.uniprot.org/core/name | "Cancer Biother Radiopharm"xsd:string |
| http://purl.uniprot.org/citations/32191537 | http://purl.uniprot.org/core/pages | "292-300"xsd:string |
| http://purl.uniprot.org/citations/32191537 | http://purl.uniprot.org/core/title | "LncRNA FOXD3-AS1 Mediates AKT Pathway to Promote Growth and Invasion in Hepatocellular Carcinoma Through Regulating RICTOR."xsd:string |
| http://purl.uniprot.org/citations/32191537 | http://purl.uniprot.org/core/volume | "35"xsd:string |
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