ArticleOncoTargets and therapy2019
CLK3 Is A Direct Target Of miR-144 And Contributes To Aggressive Progression In Hepatocellular Carcinoma.
Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- CLK3 regulates tumor angiogenesis by modulating HIF1α ubiquitination.Cancer gene therapy · 2026Article
- The alternative splicing landscape of hepatocellular carcinoma and its potential for HCC detection.Hepatology communications · 2026Article
- Unravelling the Phosphorylation Landscape of Anthrax Toxin Receptor 1: Mechanisms and Functional Insights Through Phosphoproteomic Data Integration.The protein journal · 2025Article
- CLK3 promotes tumor proliferation by activating MYC signaling.Cell division · 2024Article
- Article
- Research progress of N1-methyladenosine RNA modification in cancer.Cell communication and signaling : CCS · 2024Review
- Cdc2-like kinases: structure, biological function, and therapeutic targets for diseases.Signal transduction and targeted therapy · 2023Review
- MFAP2, upregulated by m1A methylation, promotes colorectal cancer invasiveness via CLK3.Cancer medicine · 2023Article
- Comprehensive Analysis of Colorectal Cancer Immunity and Identification of Immune-Related Prognostic Targets.Disease markers · 2022Article
- Application of RNA processing factors for predicting clinical outcomes in colon cancer.Frontiers in genetics · 2022Article
- Circular RNA hsa_circ_0000277 sequesters miR-4766-5p to upregulate LAMA1 and promote esophageal carcinoma progression.Cell death & disease · 2021Article
- Dual-Specificity, Tyrosine Phosphorylation-Regulated Kinases (DYRKs) and cdc2-Like Kinases (CLKs) in Human Disease, an Overview.International journal of molecular sciences · 2021Review
- Cdc-Like Kinases (CLKs): Biology, Chemical Probes, and Therapeutic Potential.International journal of molecular sciences · 2020Review
- Targeting CLK3 inhibits the progression of cholangiocarcinoma by reprogramming nucleotide metabolism.The Journal of experimental medicine · 2020Article
- Circ_0001175 Promotes Hepatocellular Carcinoma Cell Proliferation and Metastasis by Regulating miR-130a-5p.OncoTargets and therapy · 2020Article
- Recent progress in treatment of hepatocellular carcinoma.American journal of cancer research · 2020Review
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
backgroundHepatocellular carcinoma (HCC) is the most common type of primary liver cancer with high incidence. The underlying molecular mechanisms of HCC development have been intensively studied. CLK3 (CDC Like Kinase 3) is a nuclear dual-specificity kinase and regulates gene splicing. We investigated the expression profile and functional role of CLK3 in HCC.
methodsImmunohistochemistry (IHC) and Western blot were performed to determine CLK3 expression in HCC tissues. Bioinformatics analysis using TCGA and GEO database was conducted to evaluate the relationship between CLK3 expression and HCC prognosis. Cell proliferation was assessed by CCK8, EdU and colony formation assays, while transwell and wound-healing assays were performed to investigate the cell migration and invasion in vitro. Xenograft nude mouse model was used to test the function of CLK3 on tumor growth in vivo. Luciferase reporter assay, Western blot and RT-qPCR were conducted to verify the miRNA that directly targeted CLK3.
resultsCLK3 was markedly upregulated in HCC tissues, and the expression levels of CLK3 were closely associated with TNM stages and HCC prognosis. Functional analysis indicated that knockdown of CLK3 could suppress HCC cell growth, invasion and migration in vitro, and inhibit tumor development in vivo. Moreover, CLK3 was demonstrated as a direct target of miR-144 and miR-144 expression was inversely correlated with CLK3 expression in HCC. Enforced overexpression of miR-144 markedly inhibited the CLK3 expression while overexpression of CLK3 partially reversed the inhibitory function of miR-144 on HCC cell growth and metastasis. Mechanistically, we found that miR-144 overexpression inhibited Wnt/β-catenin signaling and the inhibition could be partly abolished by overexpression of CLK3.
conclusionIn summary, we demonstrate tumor suppressor miR-144 suppresses hepatocellular carcinoma development and metastasis via regulating CLK3 and Wnt/β-catenin signaling, indicating that miR-144/CLK3 could be used for HCC diagnosis and treatment.
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