ArticleCell cycle (Georgetown, Tex.)2012
Coordinated effects of microRNA-494 induce G₂/M arrest in human cholangiocarcinoma.
Article in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed.
- Integrated analysis reveals survival-related genes promoting cholangiocarcinoma progression via G2/M cell cycle, with validation of cyclin B1 in tumor proliferation.Scientific reports · 2025Article
- Canonical and non-canonical functions of p53 isoforms: potentiating the complexity of tumor development and therapy resistance.Cell death & disease · 2024Review
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- CDC20: a novel therapeutic target in cancer.American journal of translational research · 2023Review
- A Transcriptomic Signature for Risk-Stratification and Recurrence Prediction in Intrahepatic Cholangiocarcinoma.Hepatology (Baltimore, Md.) · 2021Article
- miR-188-5p promotes oxaliplatin resistance by targeting RASA1 in colon cancer cells.Oncology letters · 2021Article
- Hsa-miR-494-3p attenuates gene HtrA3 transcription to increase inflammatory response in hypoxia/reoxygenation HK2 Cells.Scientific reports · 2021Article
- Pathogenetic Role and Clinical Implications of Regulatory RNAs in Biliary Tract Cancer.Cancers · 2020Review
- TGF-β Enhances the Anti-inflammatory Effect of Tumor- Infiltrating CD33+11b+HLA-DR Myeloid-Derived Suppressor Cells in Gastric Cancer: A Possible Relation to MicroRNA-494.Asian Pacific journal of cancer prevention : APJCP · 2020Article
- Review
- Upregulation of cell division cycle 20 in cisplatin resistance-induced epithelial-mesenchymal transition in osteosarcoma cells.American journal of translational research · 2020Article
- A novel mouse model of orthotopic extrahepatic cholangiocarcinoma confirmed with molecular imaging.Translational cancer research · 2019Article
- Spica Prunellae Extract Enhances Fluorouracil Sensitivity of 5-Fluorouracil-Resistant Human Colon Carcinoma HCT-8/5-FU Cells via TOP2BioMed research international · 2019Article
- LncRNA PCAT6 increased cholangiocarcinoma cell proliferation and invasion via modulating miR-330-5p.American journal of translational research · 2019Article
- Survivin is a novel transcription regulator of KIT and is downregulated by miRNA-494 in gastrointestinal stromal tumors.International journal of cancer · 2018Article
- Proliferation-associated miRNAs-494, -205, -21 and -126 detected by in situ hybridization: expression and prognostic potential in breast carcinoma patients.Journal of cancer research and clinical oncology · 2018Article
- NcRNAs and Cholangiocarcinoma.Journal of Cancer · 2018Review
- Targeting theOncotarget · 2017Article
- MicroRNA-494 inhibits breast cancer progression by directly targeting PAK1.Cell death & disease · 2017Article
- MicroRNA-520d-5p inhibits human glioma cell proliferation and induces cell cycle arrest by directly targeting PTTG1.American journal of translational research · 2017Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
MicroRNA (miRs) have emerged as salient regulators in cancer homeostasis and, recently, as putative therapeutics. Cholangiocarcinomas (CCA) are aggressive cancers with survival usually measured in months. mRNA arrays followed by pathway analysis revealed that miR-494 is a major modulator of the cell cycle progression from gap 2 (G₂) to mitosis (M). We performed fluorescence activated cell sorting (FACS) as well as differential interference contrast (DIC) microscopy, and confirmed that miR-494 induces a significant arrest in G₂/M in CCA cells. Furthermore, we verified that miR-494 modulates the protein level of six genes involved in the G₂/M transition: Polo-like Kinase 1 (PLK1), pituitary tumor-transforming gene 1 (PTTG1), Cyclin B1 (CCNB1), cell-division cycle 2 (CDC2), cell-division cycle 20 (CDC20) and topoisomerase II α (TOP2A). Next, we identified direct binding of miR-494 to the open reading frame (ORF) and downregulation of PTTG1 and TOP2A. In summary, our findings suggest that miR-494 has a global regulatory role in cell cycle progression, exerted by concerted effects on multiple proteins involved in gap 1 (G₁) to synthesis (S), as described previously, as well as G₂ to M progression. Therefore, it appears that the simultaneous effects of a single miR species on multiple targets along the same canonical pathway is advantageous for the usage of miRs as therapeutics. In addition, our data suggest that miRs act within a narrow range. miR expression above the upper threshold does not appear to induce further effects, which is reassuring in terms of off-target effects of miR surrounding noncancerous tissue.
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