BEER-SHEVA, Israel, April 16, 2026 – Researchers at Ben-Gurion University of the Negev have identified a protein that plays a central role in enabling aggressive breast cancer cells to spread to other parts of the body.
Triple-negative breast cancer remains one of the most challenging diagnoses to receive. While medical advances have improved the ability to surgically remove primary tumors, the true danger lies in metastasis, which is the spread of cancer cells to vital organs like the lungs, liver, or brain. Researchers at Ben-Gurion University of the Negev have now identified a specific protein, PKC-eta (protein kinase C-eta), that drives this deadly cell migration in triple-negative breast cancer, offering a new avenue of hope for treating this aggressive disease.
The research was led by Prof. Etta Livneh and Prof. Moshe Elkabets and by their postdoctoral fellow, Liju Vijaya Steltar of the Faculty of Health Sciences at Ben-Gurion University of the Negev. Additional researchers included Dr. Ofir Cohen and others from additional BGU departments and international partners.
The findings were published in Signal Transduction and Targeted Therapy (https://doi.org/10.1038/s41392-026-02572-0).
The researchers found that PKC-eta:
• Enhances cancer cell mobility and invasiveness
• Activates gene programs that allow cancer cells to detach, migrate, and form metastases
• Binds and activates the YAP protein, a core member of the Hippo signaling pathway, which regulates metastasis.
When PKC-eta activity was reduced or eliminated in laboratory and animal models, tumors grew more slowly and showed markedly reduced metastatic spread.
"Our findings reveal that PKC-eta could represent a prognostic marker to identify patients prone to developing metastasis, and thus could serve as a therapeutic target for this highly lethal and metastatic disease," says Prof. Livneh.
The researchers combined analysis of breast cancer patient data, experiments in cancer cell lines, and animal models of tumor growth and metastatic spread.
They found that PKC-eta levels were elevated in patients' tumors with molecular features associated with poor prognosis.
However, the team went beyond identifying the problem and proposed a solution. They identified a naturally occurring peptide encoded by a sequence upstream of the PKC-eta sequence (on its mRNA) that targets and degrades PKC-eta protein. In laboratory models, introducing this peptide successfully disrupted YAP1 regulation and significantly reduced the cancer's ability to spread to the lungs and liver.
"This recently discovered peptide could be utilized as a specific therapeutic drug," according to Prof. Moshe Elkabets.
The findings are based on experimental and animal models. While PKC-eta and YAP are strongly associated with tumor aggressiveness, further research is needed to determine how these insights can be translated into clinical settings.
This research was supported by the Israel Science Foundation (grants 3280/24, 302/21, and 2802/22), the Ministry of Science, Technology and Space (grant 4981), the U.S.–Israel Binational Science Foundation (grants 2021055 and 2023129), the Ministry of Innovation, Science and Technology (grant 5912), and the Israel Cancer Research Foundation (grants 1060612 and 81233611). Additional support was provided through a Kreitman Postdoctoral Fellowship from Ben-Gurion University of the Negev.
