ArticleCell cycle (Georgetown, Tex.)2013
Lapatinib induces p27(Kip1)-dependent G₁ arrest through both transcriptional and post-translational mechanisms.
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- BDDN: bayesian dynamic differential network analysis in cancer proteomics.BMC bioinformatics · 2026Article
- Mirk/Dyrk1B Kinase Inhibitors in Targeted Cancer Therapy.Pharmaceutics · 2024Review
- Quiescent Cancer Cells-A Potential Therapeutic Target to Overcome Tumor Resistance and Relapse.International journal of molecular sciences · 2023Review
- A lineage tree-based hidden Markov model quantifies cellular heterogeneity and plasticity.Communications biology · 2022Article
- Drug-resistant HER2-positive breast cancer: Molecular mechanisms and overcoming strategies.Frontiers in pharmacology · 2022Review
- miR-221 confers lapatinib resistance by negatively regulating p27Cancer science · 2021Article
- Arctigenin-mediated cell death of SK-BR-3 cells is caused by HER2 inhibition and autophagy-linked apoptosis.Pharmacological reports : PR · 2021Article
- Minibrain-related kinase/dual-specificity tyrosine-regulated kinase 1B implication in stem/cancer stem cells biology.World journal of stem cells · 2020Review
- Self-Assembly of pH-Labile Polymer Nanoparticles for Paclitaxel Prodrug Delivery: Formulation, Characterization, and Evaluation.International journal of molecular sciences · 2020Article
- Adipocyte-conditioned medium induces resistance of breast cancer cells to lapatinib.BMC pharmacology & toxicology · 2020Article
- The DYRK Family of Kinases in Cancer: Molecular Functions and Therapeutic Opportunities.Cancers · 2020Review
- Rapid Self-Assembly of Polymer Nanoparticles for Synergistic Codelivery of Paclitaxel and Lapatinib via Flash NanoPrecipitation.Nanomaterials (Basel, Switzerland) · 2020Article
- A phase I study of HER1, HER2 dual kinase inhibitor lapatinib plus the proteasome inhibitor bortezomib in patients with advanced malignancies.Cancer chemotherapy and pharmacology · 2019Article
- Tomentosin Displays Anti-Carcinogenic Effect in Human Osteosarcoma MG-63 Cells via the Induction of Intracellular Reactive Oxygen Species.International journal of molecular sciences · 2019Article
- Foxo-dependent Par-4 Upregulation Prevents Long-term Survival of Residual Cells Following PI3K-Akt Inhibition.Molecular cancer research : MCR · 2018Article
- Effects of lapatinib on cell proliferation and apoptosis in NB4 cells.Oncology letters · 2018Article
- Epidermal Growth Factor Receptor activation promotes ADA3 acetylation through the AKT-p300 pathway.Cell cycle (Georgetown, Tex.) · 2017Article
- Butein inhibits cell proliferation and induces cell cycle arrest in acute lymphoblastic leukemia via FOXO3a/p27kip1 pathway.Oncotarget · 2016Article
- Mdig, a lung cancer-associated gene, regulates cell cycle progression through p27(KIP1).Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- TXNIP interaction with the Her-1/2 pathway contributes to overall survival in breast cancer.Oncotarget · 2015Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lapatinib, a dual EGFR/HER2 tyrosine kinase inhibitor, has been shown to have potent antitumor effects against human breast cancer. Recent studies have shown that lapatinib upregulates p27(Kip1) (here after referred to as p27) expression and induces G₁ cell cycle arrest in various types of cancer cells. However, the regulation of p27 in lapatinib-induced cell cycle arrest is not well studied. Here we demonstrate that lapatinib-induced cell growth inhibition and G₁ cell cycle arrest in HER2-overexpressing human breast cancer cells were dependent on p27. We also show that lapatinib-induced upregulation of p27 expression was mediated through both transcriptional and post-translational mechanisms. On the one hand, lapatinib treatment led to increased FOXO3a expression and enhanced p27 transcription. On the other hand, lapatinib treatment resulted in increased DYRK1B expression, which correlated with increased p27 phosphorylation at Ser10 and decreased p27 degradation. Interestingly, we found that ERβ1 but not ERβ2 expression also upregulated p27 and enhanced lapatinib-induced cell proliferation inhibition and G₁ cell cycle arrest in HER2-overexpressing breast cancer cells. Taken together, our results suggest that lapatinib induces p27 expression via both transcriptional and post-translational upregulations, leading to cell cycle arrest and cell proliferation inhibition, and that its effect on breast cancer cells may be modified by ER expression status.
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