ArticleOncotarget2016
Icaritin inhibits the expression of alpha-fetoprotein in hepatitis B virus-infected hepatoma cell lines through post-transcriptional regulation.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 52 citations in OpenAlex.
- Icaritin suppresses CAD-mediated liver cancer development by targeting miR-18b-5p in a xenograft mouse model.Medical oncology (Northwood, London, England) · 2025Article
- Article
- An overview of anti-Hepatitis B virus flavonoids and their mechanisms of action.Frontiers in cellular and infection microbiology · 2024Review
- Icaritin-elevated circ_0000190 suppresses the malignant progression of multiple myeloma by targeting miR-301a.The Kaohsiung journal of medical sciences · 2022Article
- Depleting circ_0088364 restrained cell growth and motility of human hepatocellular carcinoma via circ_0088364-miR-1270-COL4A1 ceRNA pathway.Cell cycle (Georgetown, Tex.) · 2022Article
- HBP1-mediated transcriptional repression of AFP inhibits hepatoma progression.Journal of experimental & clinical cancer research : CR · 2021Article
- Icaritin promotes apoptosis and inhibits proliferation by down-regulating AFP gene expression in hepatocellular carcinoma.BMC cancer · 2021Article
- AFP-Inhibiting Fragments for Drug Delivery: The Promise and Challenges of Targeting Therapeutics to Cancers.Frontiers in cell and developmental biology · 2021Review
- A comparative study on theDrug delivery · 2020Article
- Icaritin-induced immunomodulatory efficacy in advanced hepatitis B virus-related hepatocellular carcinoma: Immunodynamic biomarkers and overall survival.Cancer science · 2020Article
- Tumor-Derived Exosomal miR-620 as a Diagnostic Biomarker in Non-Small-Cell Lung Cancer.Journal of oncology · 2020Article
- Upregulation of microRNA-1270 suppressed human glioblastoma cancer cell proliferation migration and tumorigenesis by acting through WT1.OncoTargets and therapy · 2019Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although it has showed that icaritin can apparently suppress growth of HCC by reducing the level of AFP, the intrinsic mechanism remains unclear. In this study, we explored the possible mechanism of miRNAs on post-transcriptional regulation of AFP gene, as well as the effects of HBV infection and icaritin in hepatoma cells. The results showed that miR-620, miR-1236 and miR-1270 could bind target sites in the range of 9-18 nt and 131-151 nt downstream of the stop codon in the AFP mRNA 3'-UTR to suppress the expression of AFP. Mutation of these target sites could reverse the effects of these miRNAs. Icaritin (10 μM) might reduce the stability and translational activity of AFP mRNA by increasing the expression levels of these mentioned miRNAs. HBV infection resulted in apparent decreases of these miRNAs and, consequently, increased AFP expression. The results indicated that miR-620, miR-1236 and miR-1270 are critical factors in the post-transcriptional regulation of AFP. Icaritin can counteract the effect of HBV. These findings will contribute to full understanding of the regulatory mechanism of AFP expression in hepatoma cells. And also it revealed a synergistic mechanism of HBV infection and elevation of AFP in the pathogenesis of HCC, as well as the potential clinical significance of icaritin on the therapy of HCC induced by HBV.
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