Tier 3 — preclinical

Targeting SIRT6 epigenetically restrains neutrophil hyperplasia and enhances chemotherapeutic efficacy

Luping Wang, Xiaoqian Wu, Panxia Wang, Minshan Zhang, Li Li, Zhenhan Huang, Yang Mao, Haoming Chen, Qin Wen, Wei Liu, Zhibin Huang, Feifei Li, Juan Shen
Acta Pharmaceutica Sinica B 2026 16(8):5259-5275

Bibliography

PubMed
PMID 42592314
DOI
10.1016/j.apsb.2026.06.020

Study snapshot

DesignHigh-throughput screen, Sirt6-mutant zebrafish, leukemia models and mouse xenografts.
ModelZebrafish myeloproliferative-neoplasm model, myeloid cells and xenograft mice.
SamplePreclinical experimental cohorts.
InterventionSirt6 genetic manipulation, MDL-800 and imatinib.
DurationDisease-model treatment studies.
EndpointsNeutrophil proliferation; c-Myb expression; MPN-like phenotype; Imatinib sensitivity; Xenograft progression

What the study showed, in plain terms

SIRT6 loss promoted neutrophil hyperplasia in a zebrafish MPN-like model. MDL-800 suppressed myeloid proliferation and improved imatinib efficacy in preclinical leukemia models, adding another cancer context in which SIRT6 activation is tumor-suppressive.

Key findings

SIRT6 deacetylated H3K9 at the c-myb promoter, limiting neutrophil proliferation. MDL-800 enhanced imatinib effects and restored drug sensitivity in preclinical models.

What this study can and cannot tell us

Preclinical cancer evidence; not a human treatment trial; does not support use of consumer SIRT6 activators during cancer therapy without oncology supervision.

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Editorial review

Reviewed by the Biohack Blueprint research team

Last verified

Dr. Khaled Mahmoud, MBBChCritical Care Medicine, Longevity Science & Editorial Direction Dr. Abdulla Mostafa, PhDCellular Senescence, Neurological, Mitochondrial & Brain-Ageing Biology Dr. Amr Yasser, PhDCardiometabolic, Musculoskeletal, Gut & Bioavailability