ArticleCell death & disease2019
Akirin2 is modulated by miR-490-3p and facilitates angiogenesis in cholangiocarcinoma through the IL-6/STAT3/VEGFA signaling pathway.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 48 citations in OpenAlex.
- Unbiased profiling of translational landscape reveals TNFR2 as a translation-dependent vulnerability in colorectal cancer.Journal of experimental & clinical cancer research : CR · 2026Article
- Cancer-Associated fibroblasts regulate the development of cholangiocarcinoma through IL-6/STAT3/AKR1C3 signaling axis.Scientific reports · 2026Article
- ZBTB7A-mediated regulation of astrocytic glycolysis in neurodegenerative diseases: insights from literature review and bioinformatics prediction.Frontiers in aging neuroscience · 2026Review
- Transcranial direct current stimulation enhances the protective effect of isoflurane preconditioning on cerebral ischemia/reperfusion injury: A new mechanism associated with the nuclear protein Akirin2.CNS neuroscience & therapeutics · 2024Article
- Role of nuclear protein Akirin in the modulation of female reproduction inFrontiers in physiology · 2024Article
- Establishing Molecular Subgroups of CD8+ T Cell-Associated Genes in the Ovarian Cancer Tumour Microenvironment and Predicting the Immunotherapy Response.Biomedicines · 2023Article
- Identification of AKIRIN2 as a potential biomarker and correlation with immunotherapy in gastric adenocarcinoma by integrated bioinformatics analysis.Scientific reports · 2022Article
- Article
- Systematic Analysis of Molecular Subtypes and Immune Prediction Based on CD8 T Cell Pattern Genes Based on Head and Neck Cancer.Journal of oncology · 2022Article
- MicroRNA-490-3p and -490-5p in carcinogenesis: Separate or the same goal?Oncology letters · 2021Review
- Function of cofactor Akirin2 in the regulation of gene expression in model human Caucasian neutrophil-like HL60 cells.Bioscience reports · 2021Article
- The Role of microRNAs in Cholangiocarcinoma.International journal of molecular sciences · 2021Review
- Correlation between the Expression of Interleukin-6, STAT3, E-Cadherin and N-Cadherin Protein and Invasiveness in Nonfunctional Pituitary Adenomas.Journal of neurological surgery. Part B, Skull base · 2021Article
- Recent Advances in the Mechanism Research and Clinical Treatment of Anti-Angiogenesis in Biliary Tract Cancer.Frontiers in oncology · 2021Review
- Unraveling the molecular mechanisms between inflammation and tumor angiogenesis.American journal of cancer research · 2021Review
- Uric Acid Neuroprotection Associated to IL-6/STAT3 Signaling Pathway Activation in Rat Ischemic Stroke.Molecular neurobiology · 2021Article
- Akirin proteins in development and disease: critical roles and mechanisms of action.Cellular and molecular life sciences : CMLS · 2020Review
- Development and validation of a four-microRNA signature for placenta accreta spectrum: an integrated competing endogenous RNA network analysis.Annals of translational medicine · 2020Article
- Cholangiocarcinoma: novel therapeutic targets.Expert opinion on therapeutic targets · 2020Review
- Review
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Akirin2 is a key regulator of embryonic development and the innate immunity response. However, this regulator's role in tumorigenesis especially in cholangiocarcinoma (CCA) development has not been thoroughly elucidated to date. In the current work, we used RT-qPCR, western blot analysis, and immunohistochemistry (IHC) to explore the expression level of Akirin2, and the relationship between Akirin2 levels and clinicopathological characteristics was evaluated. The biological functions of Akirin2 were examined in vitro and in vivo by using a lentiviral vector system. Luciferase reporter assays were applied to detect the direct binding relationship between the 3'-UTR of Akirin2 mRNA and miR-490-3p. The results showed that Akirin2 was overexpressed in CCA and this upregulation was associated with a shorter overall survival. Silencing or overexpressing Akirin2 by lentiviral approaches significantly influenced CCA cell proliferation, migration, invasion, and angiogenesis. An in vivo tumor model further validated the oncogenic effect of Akirin2 on CCA cell growth, metastasis, and angiogenesis. Mechanistic studies demonstrated that Akirin2 induced angiogenesis by increasing the expression of VEGFA by activating the IL-6/STAT3 signaling pathway. Akirin2 promoted cell migratory and invasive potential by affecting the epithelial-mesenchymal transition (EMT) process. In addition, Akirin2 expression was negatively controlled by miR-490-3p in CCA cells, and miR-490-3p attenuated cell migration and angiogenesis in CCA cells by silencing Akirin2. Taken together, the data indicated that Akirin2 could be regulated by miR-490-3p at the posttranscriptional level and facilitate CCA cell progression via the IL-6/STAT3/VEGFA signaling pathway. The present study may expedite the development of novel therapeutic strategies for CCA.
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