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Updated: Jul 15, 2026

Site-Specific Lysine Lactylation via Genetic Code Expansion in E. coli and Mammalian Cells

Site-Specific Lysine Lactylation via Genetic Code Expansion in E. coli and Mammalian Cells

Published on: February 24, 2026

AIM2 Lactylation Regulates Radiotherapy Sensitivity in Triple-Negative Breast Cancer.

Jianli Chen^1,2, Ziming Zhao¹, Yangyang Xing³

¹Faculty of Chinese Medicine and State Key Laboratory of Mechanism and Quality of Chinese Medicine, Macau University of Science and Technology, Macau, People's Republic of China.

Breast Cancer (Dove Medical Press)

|July 14, 2026

Summary

Absent in melanoma 2 (AIM2) may regulate triple-negative breast cancer (TNBC) radioresistance. High lactate levels may impact AIM2 function via lactylation, affecting TNBC treatment outcomes.

Keywords:

AIM2 IRF3 lactylation radiotherapy resistance signal transduction triple-negative breast cancer

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Published on: July 21, 2018

Area of Science:

Oncology
Molecular Biology
Immunology

Background:

Triple-negative breast cancer (TNBC) is aggressive with limited therapies.
Radiotherapy is key for TNBC, but radioresistance is a major challenge.
The role of Absent in melanoma 2 (AIM2) in TNBC radioresistance and lactate microenvironment interaction is unclear.

Purpose of the Study:

Investigate AIM2's role in TNBC radioresistance.
Examine how the lactate-rich tumor microenvironment affects AIM2.
Explore the potential link between AIM2, lactate, and IRF3 in TNBC radiosensitivity.

Main Methods:

Established radiation-resistant TNBC cell models.
Utilized lentiviral transduction for AIM2 knockdown and IRF3 overexpression.
Assessed proliferation, apoptosis, protein expression, AIM2 lactylation, localization, and AIM2-IRF3 interaction via various assays.

Main Results:

Radiation increased AIM2 expression; AIM2 knockdown reduced colony formation and increased apoptosis in resistant TNBC cells.
High lactate decreased AIM2 expression, increased its lactylation and nuclear translocation.
IRF3 overexpression partially reversed AIM2 knockdown effects; lactate weakened AIM2-IRF3 interaction.

Conclusions:

AIM2 may regulate TNBC radioresistance via IRF3 interaction.
Lactate may influence this axis through AIM2 lactylation.
This suggests a mechanism linking lactate modification to TNBC radiosensitivity, requiring further validation.