[Hinews] For the first time, researchers have identified a critical role for the protein ATE1 in promoting tumor growth in breast cancer, offering new insights into potential biomarkers and targeted therapies. The findings, published in the September 2 online edition of Cell Communication and Signaling, mark a significant step forward in understanding the complex behavior of this enzyme in cancer.

ATE1, an enzyme that modifies cellular proteins through a process called arginylation, has long puzzled scientists due to its contradictory roles across different cancers. Previous studies showed that ATE1 suppresses tumors in liver and prostate cancers but promotes tumor growth in melanoma. Its function in breast cancer, however, remained unclear until now.

A research team led by Dr. Hyunjoo Cha at the Nucleic Acid Therapeutics Research Center of the Korea Research Institute of Bioscience and Biotechnology has demonstrated that ATE1 is a key driver of breast cancer cell proliferation, migration, and survival. Their study, supported by South Korea’s Ministry of Science and ICT, the National Research Foundation of Korea, and the National Conference for Science and Technology, provides compelling evidence of ATE1’s role in cancer progression.

Through genomic analysis of breast cancer patients, the team found that ATE1 is significantly overexpressed in breast cancer cells compared to healthy cells. Higher ATE1 expression was also linked to poorer treatment outcomes, suggesting its potential as a prognostic biomarker.
Group photo of Dr. Hyunjoo Cha’s research team (front row, center: Principal Investigator Dr. Hyunjoo Cha). (Photo courtesy of the Korea Research Institute of Bioscience and Biotechnology)
Group photo of Dr. Hyunjoo Cha’s research team (front row, center: Principal Investigator Dr. Hyunjoo Cha). (Photo courtesy of the Korea Research Institute of Bioscience and Biotechnology)


Further experiments in cell cultures and mouse models revealed that inhibiting ATE1 markedly reduced cancer cell growth and metastasis, while leaving normal cells largely unaffected. This selective impact highlights ATE1’s potential as a precise therapeutic target with minimal side effects.

The researchers also uncovered the mechanism behind ATE1’s role in breast cancer. Through protein signaling analysis, they showed that ATE1 activates the MAPK–MYC signaling pathway, which accelerates cancer cell growth and helps cancer cells evade apoptosis, or programmed cell death. Specifically, ATE1 stabilizes the MYC protein—a known driver of cancer proliferation—while inhibiting apoptosis, thereby fueling breast cancer progression.

These findings position ATE1 as a promising biomarker for predicting breast cancer prognosis and a potential target for novel therapies. Because ATE1 inhibition appears to spare healthy cells, it could pave the way for personalized treatments with reduced side effects, a critical consideration in cancer care.
The study, titled “ATE1 Promotes Breast Cancer Progression via Arginylation-Dependent Regulation of MAPK-MYC Signaling,” underscores the potential of ATE1-targeted strategies to transform breast cancer treatment. As researchers continue to explore its implications, this discovery could lead to more effective, tailored therapies for patients worldwide.

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