ArticleMolecular and cellular biochemistry2019
Potential of C1QTNF1-AS1 regulation in human hepatocellular carcinoma.
Article in Molecular and cellular biochemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
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- miR-221/222 as biomarkers and targets for therapeutic intervention on cancer and other diseases: A systematic review.Molecular therapy. Nucleic acids · 2022Review
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- Prognostic Significance of Alternative Splicing Genes in Cervical Squamous Cell Carcinoma and Endocervical Adenocarcinoma.International journal of general medicine · 2021Article
- Hepatoma Cell-Derived Extracellular Vesicles Promote Liver Cancer Metastasis by Inducing the Differentiation of Bone Marrow Stem Cells Through microRNA-181d-5p and the FAK/Src Pathway.Frontiers in cell and developmental biology · 2021Article
- Co-expression network analysis identifies a gene signature as a predictive biomarker for energy metabolism in osteosarcoma.Cancer cell international · 2020Article
- Long Non-Coding RNA C1QTNF1 Antisense RNA 1 Upregulates Hexokinase 2 by Sponging microRNA-484 to Promote the Malignancy of Colorectal Cancer.Cancer management and research · 2020Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of our study is to explore the regulation of C1QTNF1-AS1 on its target miR-221-3p/SOCS3 in human hepatocellular carcinoma (HCC). To explore the underlying molecular regulation of non-coding RNA for HCC, differentially expressed patterns of lncRNAs and genes were examined by RNA-seq. GO and KEGG pathway analysis were done based on the function of mRNAs that mediated by differentially expressed lncRNAs. RT-qPCR and western blot were conducted to detect the mRNA and protein level expression of C1QTNF1-AS1, miR-221-3p, SOCS3 and key proteins in JAK/STAT signaling pathway in HCC tissues and cells. The target miRNA of differentially expressed C1QTNF1-AS1 and SOCS3 was miR-221-3p predicted by bioinformatics analysis. C1QTNF1-AS1 and SOCS3 was downregulated and miR-221-3p was upregulated in HCC tissues and cells. In HepG2 and Huh-7 cells, the overexpression of C1QTNF1-AS1 or SOCS3, and silencing of miR-221-3p inhibited proliferation, migration, invasion and JAK/STAT signaling pathway, while promoted cell apoptosis. The results of dual-luciferase assay indicated that C1QTNF1-AS1 regulated miR-221-3p and miR-221-3p targeted SOCS3 by directly binding. And the growth of HCC in vivo was impeded when C1QTNF1-AS1 was upregulated. Overexpression of C1QTNF1-AS1 could downregulate miR-221-3p thereby inhibited the proliferation, migration and invasion of HCC cells.
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