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A Data Integration Workflow to Identify Drug Combinations Targeting Synthetic Lethal Interactions

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Published on: May 27, 2021

PROTAC-based synthetic lethality strategy endogenously activates systemic STING to boost antitumor immunity.

Ye Liu¹, Maolin Jiang¹, Mengchao Ding¹

¹School of Biomedical Sciences and Engineering, Guangzhou International Campus, South China University of Technology, Guangzhou 511442, P.R. China.

Science Advances

|February 27, 2026

Summary

Targeting DNA repair with PROTACs degrades PARP1 and BRD4, inducing synthetic lethality. This approach enhances STING pathway activation for potent antitumor immunity mediated by NK and T cells.

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Area of Science:

Immunology
Oncology
Molecular Biology

Background:

The stimulator of interferon genes (STING) pathway is crucial for antitumor immunity, activated by cytosolic DNA.
DNA repair mechanisms limit STING activation by preventing cytosolic DNA accumulation.
Targeting DNA repair pathways offers a potential strategy to enhance STING-mediated immunity.

Purpose of the Study:

To develop a novel therapeutic strategy using proteolysis-targeting chimeras (PROTACs) to degrade PARP1 and BRD4.
To disrupt DNA repair machinery and induce nuclear-to-cytosolic DNA leakage for enhanced STING activation.
To evaluate the antitumor efficacy and immune response elicited by this strategy.

Main Methods:

Utilized PROTACs to mediate the degradation of PARP1 and BRD4.
Induced synthetic lethality by disrupting DNA repair pathways.
Assessed STING pathway activation, immune cell infiltration (CD8+ T cells, NK cells), and tumor growth in preclinical models.
Evaluated the impact on pulmonary metastasis.

Main Results:

PROTAC-mediated degradation of PARP1 and BRD4 successfully disrupted DNA repair.
The strategy induced significant nuclear-to-cytosolic DNA leakage, surpassing the STING activation threshold.
Demonstrated superior antitumor efficacy across multiple tumor models.
Elicited robust CD8+ T cell- and NK cell-mediated antitumor immunity.
Showed suppression of pulmonary metastasis progression.

Conclusions:

The integration of synthetic lethality with PROTAC-mediated degradation of PARP1 and BRD4 is a viable strategy to enhance cGAS-STING-mediated innate immunity.
This approach overcomes limitations imposed by DNA repair machinery, leading to potent antitumor responses.
Establishes a new paradigm for leveraging STING activation in cancer immunotherapy.