ArticleScientific reports2016
FOXC2 regulates the G2/M transition of stem cell-rich breast cancer cells and sensitizes them to PLK1 inhibition.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
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- GDF10 promotes rodent cardiomyocyte maturation during the postnatal period.Journal of molecular and cellular cardiology · 2025Article
- Integrative Analysis of DNA Methylation and microRNA Reveals GNPDA1 and SLC25A16 Related to Biopsychosocial Factors Among Taiwanese Women with a Family History of Breast Cancer.Journal of personalized medicine · 2025Article
- β-Catenin Drives the FOXC2-Mediated Epithelial-Mesenchymal Transition and Acquisition of Stem Cell Properties.Cancers · 2025Article
- Spatial and Temporal Relationship between Epithelial-Mesenchymal Transition (EMT) and Stem Cells in Cancer.Clinical chemistry · 2024Article
- Stabilizing vimentin phosphorylation inhibits stem-like cell properties and metastasis of hybrid epithelial/mesenchymal carcinomas.Cell reports · 2023Article
- Proactive and reactive roles of TGF-β in cancer.Seminars in cancer biology · 2023Review
- The Role of Polo-Like Kinase 1 in Regulating the Forkhead Box Family Transcription Factors.Cells · 2023Review
- Forkhead Box Transcription Factors: Double-Edged Swords in Cancer.Cancer research · 2022Review
- miR-509 inhibits cancer stemness properties in oral carcinomas via directly targeting PlK1.Journal of dental sciences · 2022Article
- A Novel Allosteric Inhibitor Targets PLK1 in Triple Negative Breast Cancer Cells.Biomolecules · 2022Article
- Molecular targets and therapeutics in chemoresistance of triple-negative breast cancer.Medical oncology (Northwood, London, England) · 2021Review
- Gene Expression Analysis Reveals Key Genes and Signalings Associated with the Prognosis of Prostate Cancer.Computational and mathematical methods in medicine · 2021Article
- Transitional dynamics of cancer stem cells in invasion and metastasis.Translational oncology · 2021Review
- FOXC2 Promotes Oxaliplatin Resistance by Inducing Epithelial-Mesenchymal Transition via MAPK/ERK Signaling in Colorectal Cancer.OncoTargets and therapy · 2020Article
- Phosphorylation of the histone demethylase KDM5B and regulation of the phenotype of triple negative breast cancer.Scientific reports · 2019Article
- Role and importance of the expression of transcription factor FOXC2 in cervical cancer.Oncology letters · 2017Article
- MicroRNA Let-7g Directly Targets Forkhead Box C2 (FOXC2) to Modulate Bone Metastasis in Breast Cancer.Open medicine (Warsaw, Poland) · 2017Article
- The Emerging Roles of Forkhead Box (FOX) Proteins in Osteosarcoma.Journal of Cancer · 2017Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Cancer cells with stem cell properties (CSCs) underpin the chemotherapy resistance and high therapeutic failure of triple-negative breast cancers (TNBCs). Even though CSCs are known to proliferate more slowly, they are sensitive to inhibitors of G2/M kinases such as polo-like kinase 1 (PLK1). Understanding the cell cycle regulatory mechanisms of CSCs will help target these cells more efficiently. Herein, we identify a novel role for the transcription factor FOXC2, which is mostly expressed in CSCs, in the regulation of cell cycle of CSC-enriched breast cancer cells. We demonstrate that FOXC2 expression is regulated in a cell cycle-dependent manner, with FOXC2 protein levels accumulating in G2, and rapidly decreasing during mitosis. Knockdown of FOXC2 in CSC-enriched TNBC cells delays mitotic entry without significantly affecting the overall proliferation rate of these cells. Moreover, PLK1 activity is important for FOXC2 protein stability, since PLK1 inhibition reduces FOXC2 protein levels. Indeed, FOXC2 expressing CSC-enriched TNBC cells are sensitive to PLK1 inhibition. Collectively, our findings demonstrate a novel role for FOXC2 as a regulator of the G2/M transition and elucidate the reason for the observed sensitivity of CSC-enriched breast cancer cells to PLK1 inhibitor.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.