Related Experiment Video
Updated: Aug 9, 2025

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment
Published on: June 9, 2023
Inhibition of Polo-like kinase 1 (PLK1) triggers cell apoptosis via ROS-caused mitochondrial dysfunction in
Ya Feng1, Tianjiao Li1, Zhoujun Lin1
1State Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, Nankai University, No. 38 Tongyan Road, Jinnan District, Tianjin, 300350, People's Republic of China.
Background:
Colorectal 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.
Methods:
GEPIA 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.
Results:
First, 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.
Conclusion:
These 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.
Insights
Polo-like kinase 1 (PLK1) inhibition reduces colorectal cancer (CRC) cell viability and migration. This study highlights PLK1 as a promising therapeutic target for CRC treatment, with BI6727 showing potential.
Area of Science:
- Oncology
- Cell Biology
- Molecular Biology
Background:
- Colorectal cancer (CRC) is a prevalent malignancy with poorly understood non-mitotic roles of Polo-like kinase 1 (PLK1).
- PLK1 is crucial for cell cycle regulation, including chromosome segregation, centrosome maturation, and cytokinesis.
Purpose of the Study:
- To investigate the tumorigenic effects of PLK1 in colorectal cancer.
- To explore the potential of PLK1 as a therapeutic target for CRC treatment.
Main Methods:
- Utilized GEPIA database and immunohistochemistry to assess PLK1 expression in CRC.
- Employed RNAi and the small molecule inhibitor BI6727 to inhibit PLK1.
- Assessed cell viability, migration, apoptosis, mitochondrial membrane potential, and ROS levels using MTT, colony formation, transwell, and flow cytometry assays.
- Evaluated PLK1 inhibition effects in preclinical models, including bioluminescence imaging and xenograft tumor models.
Main Results:
- PLK1 was significantly accumulated in CRC tissues compared to adjacent healthy tissues.
- PLK1 inhibition reduced CRC cell viability, migration, and colony formation, while inducing apoptosis.
- PLK1 inhibition led to increased ROS, decreased Bcl2/Bax ratio, mitochondrial dysfunction, and Cytochrome c release, initiating apoptosis.
Conclusions:
- PLK1 plays a significant role in CRC pathogenesis.
- PLK1 inhibition demonstrates therapeutic potential for CRC.
- The PLK1 inhibitor BI6727 represents a potential novel therapeutic strategy for colorectal cancer.
More Related Videos
Related Concept Videos
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
The Intrinsic Apoptotic Pathway
PI3K/mTOR/AKT Signaling Pathway
Abnormal Proliferation
Electron Transport Chain: Complex I and II
ROS generation is regulated and maintained at moderate levels necessary...
Inhibition of Cdk Activity

