ArticleJournal of cancer research and clinical oncology2023
Inhibition of Polo-like kinase 1 (PLK1) triggers cell apoptosis via ROS-caused mitochondrial dysfunction in colorectal carcinoma.
Article in Journal of cancer research and clinical oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Dysregulated TMPO-AS1/let-7b-5p/PLK1/E2F1 Axis Associated with Poor Prognosis in Lung Adenocarcinoma.Asian Pacific journal of cancer prevention : APJCP · 2026Article
- Proteomics and phosphoproteomics of human colorectal cancer cells lacking a specific kinase activity reveal kinase-specific compensatory responses.Animal cells and systems · 2026Article
- Resveratrol-Curcumin Hybrid Selectively Induces Chromosomal Abnormalities and Apoptosis in Colon Adenocarcinoma Cells.Antioxidants (Basel, Switzerland) · 2025Article
- Identification of targetable vulnerabilities of PLK1-overexpressing cancers by synthetic dosage lethality.Cell genomics · 2025Article
- Structural regulation of PLK1 activity: implications for cell cycle function and drug discovery.Cancer gene therapy · 2025Review
- Onvansertib inhibits cell proliferation and increases sensitivity to paclitaxel in uterine serous cancer cells.American journal of cancer research · 2025Article
- PLK1 inhibition impairs erythroid differentiation.Frontiers in cell and developmental biology · 2024Article
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundColorectal cancer (CRC) is one of the most frequently diagnosed cancers. Polo-like kinase 1 (PLK1), a member of the serine/threonine kinase PLK family, is the most investigated and essential in the regulation of cell cycle progression, including chromosome segregation, centrosome maturation and cytokinesis. However, the nonmitotic role of PLK1 in CRC is poorly understood. In this study, we explored the tumorigenic effects of PLK1 and its potential as a therapeutic target in CRC.
methodsGEPIA database and immunohistochemistry analysis were performed to evaluate the abnormal expression of PLK1 in CRC patients. MTT assay, colony formation and transwell assay were performed to assess cell viability, colony formation ability and migration ability after inhibiting PLK1 by RNAi or the small molecule inhibitor BI6727. Cell apoptosis, mitochondrial membrane potential (MMP) and ROS levels were evaluated by flow cytometry. Bioluminescence imaging was performed to evaluate the impact of PLK1 on CRC cell survival in a preclinical model. Finally, xenograft tumor model was established to study the effect of PLK1 inhibition on tumor growth.
resultsFirst, immunohistochemistry analysis revealed the significant accumulation of PLK1 in patient-derived CRC tissues compared with adjacent healthy tissues. Furthermore, PLK1 inhibition genetically or pharmacologically significantly reduced cell viability, migration and colony formation, and triggered apoptosis of CRC cells. Additionally, we found that PLK1 inhibition elevated cellular reactive oxygen species (ROS) accumulation and decreased the Bcl2/Bax ratio, which led to mitochondrial dysfunction and the release of Cytochrome c, a key process in initiating cell apoptosis.
conclusionThese data provide new insights into the pathogenesis of CRC and support the potential value of PLK1 as an appealing target for CRC treatment. Overall, the underlying mechanism of inhibiting PLK1-induced apoptosis indicates that the PLK1 inhibitor BI6727 may be a novel potential therapeutic strategy in the treatment of CRC.
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