SIRT7-mediated deacetylation of XRCC6 at lysine 591 drives breast cancer progression
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By
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Jie Yin
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Jiaxing Liu
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Meirui He
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Tang Xiao
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Wenjuan Xiang
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Ruxia Sheng
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Haifang Zhao
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Xinyue Huang
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Sheng Xu
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Yong Zhou
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Junfeng Liu
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Ruijuan Heng
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Xiaoying He
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Yunxiang Wang
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Yu Song
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Pan Qi
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May 8, 2026
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Clinical Scorecard: The Role of SIRT7 in the Deacetylation of XRCC6 at Lysine 591 and Its Impact on Breast Cancer Progression
At a Glance
| Category | Detail |
|---|
| Condition | Breast Cancer |
| Key Mechanisms | Downregulation of XRCC6 acetylation at K591 enhances DNA damage repair and promotes tumor growth. |
| Target Population | Patients with breast cancer |
| Care Setting | Clinical oncology |
Key Highlights
- XRCC6 acetylation is significantly reduced in breast cancer tissues compared to paracancerous tissues.
- Sirt7 is identified as the specific deacetylase for XRCC6.
- Downregulated XRCC6 acetylation promotes tumor growth in xenograft models.
- EP300 is the acetyltransferase responsible for XRCC6 acetylation.
- Alterations in XRCC6 acetylation impact DNA damage repair capacity.
Guideline-Based Recommendations
Diagnosis
- Assess acetylation levels of XRCC6 in breast cancer tissues.
Management
- Consider targeting XRCC6 acetylation pathways for therapeutic strategies.
Monitoring & Follow-up
- Monitor tumor growth and DNA repair capacity in relation to XRCC6 acetylation status.
Risks
- Increased tumor growth and genomic instability associated with reduced XRCC6 acetylation.
Patient & Prescribing Data
Breast cancer patients with altered XRCC6 acetylation.
Targeting Sirt7 or EP300 may provide new therapeutic avenues.
Clinical Best Practices
- Utilize acetylproteomics for evaluating protein modifications in cancer.
- Incorporate assessments of XRCC6 function in treatment planning.
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