ArticleCell communication and signaling : CCS2019
Inhibition of cyclin E1 sensitizes hepatocellular carcinoma cells to regorafenib by mcl-1 suppression.
Article in Cell communication and signaling : CCS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 28 citations in OpenAlex.
- Comparison of the Effects of Sorafenib and Stem Cell Secretome on HepG2 Cancer Cells with Respect to the Ras/Raf/MEK/ERK Pathway.Journal of clinical medicine · 2026Article
- PROTACs: Current and Future Potential as a Precision Medicine Strategy to Combat Cancer.Molecular cancer therapeutics · 2024Review
- Integrative proteogenomic characterization of hepatocellular carcinoma across etiologies and stages.Nature communications · 2022Review
- FBXL16 Promotes Endometrial Progesterone Resistance via PP2AJournal of immunology research · 2022Article
- Nanomedicine in Hepatocellular Carcinoma: A New Frontier in Targeted Cancer Treatment.Pharmaceutics · 2021Review
- Cyclin E1 in Murine and Human Liver Cancer: A Promising Target for Therapeutic Intervention during Tumour Progression.Cancers · 2021Article
- Identification of hub genes associated with prognosis, diagnosis, immune infiltration and therapeutic drug in liver cancer by integrated analysis.Human genomics · 2021Article
- Targeting transcription of MCL-1 sensitizes HER2-amplified breast cancers to HER2 inhibitors.Cell death & disease · 2021Article
- Long non-coding RNA ELDR enhances oral cancer growth by promoting ILF3-cyclin E1 signaling.EMBO reports · 2020Article
- Targeted therapy for hepatocellular carcinoma.Signal transduction and targeted therapy · 2020Review
- Article
- OTUB1 Promotes Progression and Proliferation of Prostate Cancer via Deubiquitinating and Stabling Cyclin E1.Frontiers in cell and developmental biology · 2020Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTo clarify the effects of cylcin E1 expression on HCC tumor progression, we studied the expression of cyclin E1 and inhibitory efficacy of regorafenib and sorafenib in HCC cells, and investigated a potential therapy that combines regorafenib treatment with cyclin E1 inhibition.
methodsWestern blotting for caspase-3 and Hoechst 33225 staining was used to measure the expression level of apoptosis-related proteins under drug treatment.
resultsOur results showed that enhanced expression of cyclin E1 after transfection compromised apoptosis in HCC cells induced by regorafenib or sorafenib. Conversely, down-regulation of cyclin E1 gene expression or inhibition of cyclin E1 by the cyclin-dependent kinase (CDK) inhibitors dinaciclib (DIN) or flavopiridol sensitized HCC cells to regorafenib and sorafenib by inducing apoptosis. The expression of Mcl-1, which is modulated by STAT3, plays a key role in regulating the therapeutic effects of CDK inhibitors. Xenograft experiments conducted to test the efficacy of regorafenib combined with DIN showed dramatic tumor inhibitory effects due to induction of apoptosis. Our results suggested that the level of cyclin E1 expression in HCCs may be used as a pharmacodynamic biomarker to assess the antitumor effects of regorafenib or sorafenib.
conclusionsCombining regorafenib and CDK inhibitors may enhance the clinical efficiency of the treatment of HCCs.
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