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PLK1 and FoxM1 expressions positively correlate in papillary thyroid carcinoma and their combined inhibition results
Pratheesh Kumar Poyil1, Abdul K Siraj1, Divya Padmaja1
1Human Cancer Genomic Research, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia.
Molecular Oncology
|February 16, 2024
Summary
Polo-like kinase 1 (PLK1) is overexpressed in papillary thyroid carcinoma (PTC) and linked to poor prognosis. Targeting PLK1 and FoxM1 together shows promise for treating aggressive PTC.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Polo-like kinase 1 (PLK1) is crucial for cell proliferation and mitosis.
- PLK1 plays a significant role in various cancers, including thyroid carcinoma.
Purpose of the Study:
- To investigate the role of PLK1 in papillary thyroid carcinoma (PTC).
- To explore the correlation between PLK1 and forkhead box protein M1 (FoxM1) in PTC.
- To evaluate the therapeutic potential of targeting PLK1 and FoxM1 in PTC.
Main Methods:
- Analysis of PLK1 protein expression in PTC patient samples.
- In vitro and in vivo studies using PTC cell lines.
- Immunoprecipitation to assess PLK1-FoxM1 interaction.
- Treatment with PLK1 and FoxM1 inhibitors.
Main Results:
- PLK1 overexpression was found in 54.2% of PTC cases and correlated with aggressive features and poor prognosis.
- PLK1 inhibition reduced PTC cell proliferation, induced cell cycle arrest and apoptosis, and decreased spheroid self-renewal.
- PLK1 directly interacts with FoxM1, with PLK1 regulating FoxM1 expression.
- Combined inhibition of PLK1 and FoxM1 exhibited synergistic effects on PTC cell growth and tumor progression.
Conclusions:
- PLK1 is a significant driver of PTC tumorigenesis and a prognostic marker.
- The PLK1-FoxM1 pathway is critical in PTC development.
- Dual targeting of PLK1 and FoxM1 presents a promising therapeutic strategy for aggressive PTC.
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