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http://purl.uniprot.org/citations/31863778http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/31863778http://www.w3.org/2000/01/rdf-schema#comment"

Objective

Accumulating Studies implies that long-chain non-coding RNA (lncRNA) plays a vital regulatory role in the occurrence and progression of tumors. This study aimed to explore the function and mechanism of lncRNA HLA-F antisense RNA 1 (HLA-F-AS1) in colorectal cancer (CRC).

Methods

Expressions of HLA-F-AS1, miR-330-3p and profilin 1 (PFN1) mRNA in CRC tissues were detected by RT-PCR. MTT assay was used to detect cell proliferation, and Transwell assay was used to detect cell migration and invasion. In addition, PFN1 and apoptosis-related protein Bcl-2 associated X (Bax) and B cell lymphoma/leukmia-2 (Bcl2) were detected by western blot. Interactions between miR-330-3p and HLA-F-AS1 or the 3'UTR of PFN1 were predicted and determined by bioinformatics analysis and luciferase reporter assay.

Results

Expressions of HLA-F-AS1 and PFN1 were significantly up-regulated while miR-330-3p was significantly down-regulated in CRC tissues and cell lines. Over-expressions of HLA-F-AS1 or transfection of miR-330-3p inhibitors could promote the proliferation, migration and invasion and block apoptosis of CRC cells, whereas knockdown of HLA-F-AS1 or transfection of miR-330-3p mimics led to the opposite effects. Additionally, HLA-F-AS1 could down-regulate miR-330-3p via sponging it. HLA-F-AS1 also enhanced the expressions of PFN1, which was validated as a target gene of miR-330-3p.

Conclusion

HLA-F-AS1 promoted CRC progression via regulating miR-330-3p/PFN1 axis."xsd:string
http://purl.uniprot.org/citations/31863778http://purl.org/dc/terms/identifier"doi:10.1016/j.lfs.2019.117180"xsd:string
http://purl.uniprot.org/citations/31863778http://purl.uniprot.org/core/author"Huang Y."xsd:string
http://purl.uniprot.org/citations/31863778http://purl.uniprot.org/core/author"Liu Z."xsd:string
http://purl.uniprot.org/citations/31863778http://purl.uniprot.org/core/author"Ma X."xsd:string
http://purl.uniprot.org/citations/31863778http://purl.uniprot.org/core/author"Sun H."xsd:string
http://purl.uniprot.org/citations/31863778http://purl.uniprot.org/core/author"Pan Y."xsd:string
http://purl.uniprot.org/citations/31863778http://purl.uniprot.org/core/author"Yu D."xsd:string
http://purl.uniprot.org/citations/31863778http://purl.uniprot.org/core/author"Zeng Y."xsd:string
http://purl.uniprot.org/citations/31863778http://purl.uniprot.org/core/author"Xiang Y."xsd:string
http://purl.uniprot.org/citations/31863778http://purl.uniprot.org/core/date"2020"xsd:gYear
http://purl.uniprot.org/citations/31863778http://purl.uniprot.org/core/name"Life Sci"xsd:string
http://purl.uniprot.org/citations/31863778http://purl.uniprot.org/core/pages"117180"xsd:string
http://purl.uniprot.org/citations/31863778http://purl.uniprot.org/core/title"HLA-F-AS1/miR-330-3p/PFN1 axis promotes colorectal cancer progression."xsd:string
http://purl.uniprot.org/citations/31863778http://purl.uniprot.org/core/volume"254"xsd:string
http://purl.uniprot.org/citations/31863778http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/31863778
http://purl.uniprot.org/citations/31863778http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/31863778
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