ArticleCancer cell international2018
MicroRNA-10b regulates epithelial-mesenchymal transition by modulating KLF4/KLF11/Smads in hepatocellular carcinoma.
Article in Cancer cell international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- MicroRNA panels as diagnostic biomarkers for colorectal cancer: A systematic review and meta-analysis.Frontiers in medicine · 2022Pooled it
- Alterations of Krüppel-like Factor Signaling and Potential Targeted Therapy for Hepatocellular Carcinoma.Anti-cancer agents in medicinal chemistry · 2025Review
- Systematic integration of molecular and clinical approaches in HCV-induced hepatocellular carcinoma.Journal of translational medicine · 2024Article
- miRNA and lncRNA as potential tissue biomarkers in hepatocellular carcinoma.Non-coding RNA research · 2024Review
- The induction of ferroptosis by KLF11/NCOA4 axis: the inhibitory role in clear cell renal cell carcinoma.Human cell · 2023Article
- Deregulation of the miR-19b/PPP2R5E Signaling Axis Shows High Functional Impact in Colorectal Cancer Cells.International journal of molecular sciences · 2023Article
- Current research advances in microRNA-mediated regulation of Krüppel-like factor 4 in cancer: a narrative review.Annals of translational medicine · 2021Review
- miR-155 promotes proliferation and epithelial-mesenchymal transition of MCF-7 cells.Experimental and therapeutic medicine · 2021Article
- Long non‑coding RNA MEG3 inhibits cell migration and invasion of non‑small cell lung cancer cells by regulating the miR‑21‑5p/PTEN axis.Molecular medicine reports · 2021Article
- Recent Discoveries on the Involvement of Krüppel-Like Factor 4 in the Most Common Cancer Types.International journal of molecular sciences · 2020Review
- The Distinct Roles of Transcriptional Factor KLF11 in Normal Cell Growth Regulation and Cancer as a Mediator of TGF-β Signaling Pathway.International journal of molecular sciences · 2020Review
- Review
- Effect and mechanism of microRNA-10b on proliferation and invasion of esophageal cancer cells.Experimental and therapeutic medicine · 2019Article
- Review
- Regulation of Krüppel-Like Factor 4 (KLF4) expression through the transcription factor Yin-Yang 1 (YY1) in non-Hodgkin B-cell lymphoma.Oncotarget · 2019Article
- Emerging microRNA biomarkers for colorectal cancer diagnosis and prognosis.Open biology · 2019Review
- microRNA-16 Via Twist1 Inhibits EMT Induced by PM2.5 Exposure in Human Hepatocellular Carcinoma.Open medicine (Warsaw, Poland) · 2019Article
- MiR-125a-5p promotes osteoclastogenesis by targeting TNFRSF1B.Cellular & molecular biology letters · 2019Article
- Serum starvation induces cell death in NSCLC via miR-224.OncoTargets and therapy · 2019Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOur previous work showed that miR-10b was overexpressed in hepatocellular carcinoma (HCC) and promoted HCC cell migration and invasion. Epithelial-mesenchymal transition (EMT) is involved in HCC metastasis. So, we suspected that miR-10b might participate in the HCC EMT.
methodsWe performed morphological analysis and immunofluorescence to observe the roles of miR-10b in HCC EMT. The expression of KLF11 and EMT markers were detected by real-time RT-PCR and western blot. The regulation roles of miR-10b on KLF11 and KLF4 were determined by luciferase reporter assay. The chromatin immunoprecipitation revealed the binding relationship between KLF4 and KLF11.
resultsWe found that overexpression of miR-10b could promote HCC EMT. miR-10b could upregulated KLF11 expression. The upregulation of KLF11 reduced the downstream molecular Smad7 expression, which upregulated the Smad3 expression to promote EMT development. Furthermore, the induction role of miR-10b in HCC EMT could be blocked by KLF11 siRNA. But our results showed that there was no direct regulation of miR-10b in KLF11 expression. Specifically, miR-10b could bind to the 3'UTR of KLF4 and inhibit KLF4 expression. KLF4 could directly bind to KLF11 promoter and downregulate KLF11 transcription.
conclusionOur results reveal that miR-10b downregulates KLF4, the inhibitory transcriptional factor of KLF11, which induces Smads signaling activity to promote HCC EMT. Our study presents the regulation mechanism of miR-10b in EMT through the KLF4/KLF11/Smads pathway for the first time and implicates miR-10b as a potential target for HCC therapies.
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