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Updated: Apr 23, 2026
Impedance-based Real-time Measurement of Cancer Cell Migration and Invasion
Published on: April 2, 2020
Stable SET knockdown in breast cell carcinoma inhibits cell migration and invasion
Jie Li1, Xi-fei Yang2, Xiao-hu Ren1
1Department of Occupational Health and Occupational Medicine, School of Public Health and Tropical Medicine, Southern Medical University, Guangzhou, China; Key Laboratory of Modern Toxicology of Shenzhen, Shenzhen Center for Disease Control and Prevention, Shenzhen, China.
Abstract:
Breast cancer is the most malignant tumor for women, however, the mechanisms underlying this devastating disease remain unclear. SET is an endogenous inhibitor of protein phosphatase 2A (PP2A) and involved in many physiological and pathological processes. SET could promote the occurrence of tumor through inhibiting PP2A. In this study, we explore the role of SET in the migration and invasion of breast cancer cells MDA-MB-231 and ZR-75-30. The stable suppression of SET expression through lentivirus-mediated RNA interference (RNAi) was shown to inhibit the growth, migration and invasion of breast cancer cells. Knockdown of SET increases the activity and expression of PP2Ac and decrease the expression of matrix metalloproteinase 9 (MMP-9). These data demonstrate that SET may be involved in the pathogenic processes of breast cancer, indicating that SET can serve as a potential therapeutic target for the treatment of breast cancer.
Insights
The study reveals that inhibiting SET protein expression significantly reduces breast cancer cell growth, migration, and invasion. This finding highlights SET as a potential therapeutic target for breast cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Breast cancer remains a leading cause of mortality in women, with underlying mechanisms requiring further elucidation.
- SET protein acts as an endogenous inhibitor of protein phosphatase 2A (PP2A), potentially promoting tumor development by suppressing PP2A activity.
Purpose of the Study:
- To investigate the role of SET protein in the migration and invasion of human breast cancer cell lines (MDA-MB-231 and ZR-75-30).
- To assess the therapeutic potential of targeting SET in breast cancer.
Main Methods:
- Utilized lentivirus-mediated RNA interference (RNAi) for stable suppression of SET expression in breast cancer cells.
- Quantified changes in cell growth, migration, and invasion.
- Assessed the activity and expression of protein phosphatase 2A catalytic subunit (PP2Ac) and matrix metalloproteinase 9 (MMP-9).
Main Results:
- Stable suppression of SET expression via RNAi inhibited the growth, migration, and invasion of breast cancer cells.
- Knockdown of SET led to increased PP2Ac activity and expression.
- SET knockdown resulted in decreased expression of matrix metalloproteinase 9 (MMP-9).
Conclusions:
- SET protein plays a significant role in the pathogenic processes of breast cancer, specifically in cell migration and invasion.
- Targeting SET presents a potential therapeutic strategy for breast cancer treatment due to its role in promoting tumor progression.
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