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Updated: Feb 9, 2026

Invasive Behavior of Human Breast Cancer Cells in Embryonic Zebrafish
Published on: April 25, 2017
Knockdown of KIF26B inhibits breast cancer cell proliferation, migration, and invasion
Shudong Gu1, Haibin Liang2, Donghui Qi3
1Department of Oncology, Affiliated Hospital of Nantong University, Nantong 226001, China.
Background:
Kinesin family member 26B (KIF26B) plays a key role in the development and progression of many human cancers. However, the role and underlying mechanisms of KIF26B in breast cancer cells remain unknown.
Materials And Methods:
In this study, we inhibited the expression of KIF26B in MDA-MB-231 and MCF-7 cells using lentivirus-delivered shRNA.
Results:
Lentivirus-mediated KIF26B knockdown significantly suppressed cell proliferation, colony formation, migration, and invasion. Furthermore, cell cycle analyses revealed that the percentage of cells in the G0/G1 phase was significantly increased in KIF26B knockdown cells. Moreover, the knockdown of KIF26B significantly promoted cell apoptosis via the upregulation of cleaved caspase-3 and Bax.
Conclusion:
Our data indicate that KIF26B plays a pivotal role in tumor growth and metastasis in breast cancer cells and may be a potential therapeutic target for treating breast cancer.
Insights
Kinesin family member 26B (KIF26B) inhibition suppressed breast cancer cell growth, migration, and invasion. Knockdown promoted apoptosis and cell cycle arrest, suggesting KIF26B as a therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Kinesin family member 26B (KIF26B) is implicated in various human cancers.
- The specific role of KIF26B in breast cancer remains unclear.
Purpose of the Study:
- To investigate the function and mechanisms of KIF26B in breast cancer cells.
- To assess the potential of KIF26B as a therapeutic target.
Main Methods:
- KIF26B expression was inhibited in MDA-MB-231 and MCF-7 breast cancer cell lines using lentivirus-delivered shRNA.
- Cell proliferation, colony formation, migration, invasion, cell cycle, and apoptosis were analyzed.
Main Results:
- KIF26B knockdown significantly inhibited cell proliferation, colony formation, migration, and invasion.
- KIF26B inhibition led to increased G0/G1 phase cell cycle arrest.
- KIF26B knockdown promoted apoptosis, evidenced by increased cleaved caspase-3 and Bax expression.
Conclusions:
- KIF26B plays a critical role in breast cancer tumor growth and metastasis.
- KIF26B represents a potential therapeutic target for breast cancer treatment.
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