ArticleCell death & disease2018
MiR-126 negatively regulates PLK-4 to impact the development of hepatocellular carcinoma via ATR/CHEK1 pathway.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 86 citations in OpenAlex.
- miRNA-mediated cell-to-cell communications boost DNA repair during the radioadaptive response.Nucleic acids research · 2026Article
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- MicroRNA-126 (MiR-126): key roles in related diseases.Journal of physiology and biochemistry · 2024Review
- The prognostic values and immune characteristics of polo-like kinases (PLKs) family: A pan-cancer multi-omics analysis.Heliyon · 2024Article
- Centrosome amplification-related signature correlated with immune microenvironment and treatment response predicts prognosis and improves diagnosis of hepatocellular carcinoma by integrating machine learning and single-cell analyses.Hepatology international · 2024Article
- The role of microRNAs in hepatocellular carcinoma: Therapeutic targeting of tumor suppressor and oncogenic genes.Clinical and experimental hepatology · 2023Review
- Expressional and functional characteristics of checkpoint kinase 1 as a prognostic biomarker in hepatocellular carcinoma.Translational cancer research · 2022Article
- miR-126 downregulates CXCL12 expression in intestinal epithelial cells to suppress the recruitment and function of macrophages and tumorigenesis in a murine model of colitis-associated colorectal cancer.Molecular oncology · 2022Article
- Polo-like kinase 4 is associated with advanced TNM stages and reduced survival and its inhibition improves chemosensitivity in colorectal cancer.Oncology letters · 2022Article
- CBX3 regulated by miR-139 promotes the development of HCC by regulating cell cycle progression.Cell cycle (Georgetown, Tex.) · 2022Article
- Upstream open reading frames control PLK4 translation and centriole duplication in primordial germ cells.Genes & development · 2022Article
- Identification of a Novel Survival-Related circRNA-miRNA-mRNA Regulatory Network Related to Immune Infiltration in Liver Hepatocellular Carcinoma.Frontiers in genetics · 2022Article
- Downregulation of METTL6 mitigates cell progression, migration, invasion and adhesion in hepatocellular carcinoma by inhibiting cell adhesion molecules.International journal of oncology · 2022Article
- Identification and assessment of PLK1/2/3/4 in lung adenocarcinoma and lung squamous cell carcinoma: Evidence from methylation profile.Journal of cellular and molecular medicine · 2021Article
- Cytokinesis regulators as potential diagnostic and therapeutic biomarkers for human hepatocellular carcinoma.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- Current Implications of microRNAs in Genome Stability and Stress Responses of Ovarian Cancer.Cancers · 2021Review
- Review
- Long Noncoding RNA TCONS_00068220 Promotes Breast Cancer Progression by Regulating Epithelial-Mesenchymal Transition Marker E-Cadherin.Medical science monitor : international medical journal of experimental and clinical research · 2021Article
- Dynamics of m6A RNA Methylome on the Hallmarks of Hepatocellular Carcinoma.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging evidence has shown that microRNA-126 (miR-126) is aberrantly downregulated and plays a vital role in carcinogenesis in various cancers, including HCC. However, the underlying biological mechanisms of miR-126 in HCC are still largely unknown. In present study, we found that miR-126 was downregulated both in HCC tissues and cell lines. Low expression level of miR-126 was associated with poor overall survival (OS), late TNM stage and the presence of recurrence. Overexpression of miR-126 significantly decreased cell proliferation, metastasis and promoted apoptosis in vitro. Additional, high miR-126 expression reduced the tumor growth in vivo. Further we discovered that PLK (polo-like kinases)-4, a critical regulator in cell cycle, was a target of miR-126. PLK-4 overexpression could rescue the inhibitory effects of miR-126 on cell proliferation and invasion. Moreover, PLK-4 mRNA and protein levels were significantly upregulated in HCC tissues and positively associated with malignancies and poor OS. Knockdown PLK-4 significantly inhibited cell proliferation, invasion and promoted cell apoptosis in vitro whereas decreased tumor growth in vivo. More importantly, bioinformatics analysis combined with validation experiments in vitro and in vivo showed that activation of the ATR/CHEK1 pathway was involved in the oncogenic functions of PLK4 in HCC. We also validated that PLK4 could directly interact with ATR through CoIP assay. Taken together, we demonstrate that miRNA-126/PLK-4 axis is critical for tumorigenesis and progression of HCC, and the newly identified PLK-4/ATR/CHEK1 pathway may be a potential therapeutic target for HCC treatment.
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