Exploring the Single-Cell Dynamics of FOXM1 Under Cell Cycle Perturbations
Issued Date
2025-01-01
Resource Type
ISSN
09607722
eISSN
13652184
Scopus ID
2-s2.0-105000450397
Journal Title
Cell Proliferation
Rights Holder(s)
SCOPUS
Bibliographic Citation
Cell Proliferation (2025)
Suggested Citation
Jawwad T., Kamkaew M., Phongkitkarun K., Chusorn P., Jamnongsong S., Lam E.W.F., Sampattavanich S. Exploring the Single-Cell Dynamics of FOXM1 Under Cell Cycle Perturbations. Cell Proliferation (2025). doi:10.1111/cpr.70019 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/108558
Title
Exploring the Single-Cell Dynamics of FOXM1 Under Cell Cycle Perturbations
Author's Affiliation
Corresponding Author(s)
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Abstract
The cell cycle is crucial for maintaining normal cellular functions and preventing replication errors. FOXM1, a key transcription factor, plays a pivotal role in regulating cell cycle progression and is implicated in various physiological and pathological processes, including cancers like liver, prostate, breast, lung and colon cancer. Despite previous research, our understanding of FOXM1 dynamics under different cell cycle perturbations and its connection to heterogeneous cell fate decisions remains limited. In this study, we investigated FOXM1 behaviour in individual cells exposed to various perturbagens. We found that different drugs induce diverse responses due to heterogeneous FOXM1 dynamics at the single-cell level. Single-cell analysis identified six distinct cellular phenotypes: on-time cytokinesis, cytokinesis delay, cell cycle delay, G1 arrest, G2 arrest and cell death, observed across different drug types and doses. Specifically, treatments with PLK1, CDK1, CDK1/2 and Aurora kinase inhibitors revealed varied FOXM1 dynamics leading to heterogeneous cellular outcomes. Our findings affirm that the dynamics of FOXM1 are essential in shaping cellular outcomes, influencing the signals that dictate responses to various stimuli. Our results gave insights into how FOXM1 dynamics contribute to cell cycle fate decisions, especially under different cell cycle perturbations.
