Reprogramming Postablation Tumor Immune Microenvironment with Dual-Function Nanotherapeutic Immunomodulator for Synergistic Antitumor Immunity and Recurrence Suppression

Radiofrequency ablation (RFA) has emerged as a predominant minimally invasive approach for liver tumors, achieving favorable therapeutic outcomes and triggering a systemic immune response via the release of tumor-associated antigens. However, postablation tumor recurrence remains a critical challenge in clinics. Our previous studies revealed that ablation-induced immunosuppression, primarily characterized by the expansion and activation of myeloid-derived suppressor cells (MDSCs), critically compromised the host's antitumor immunity, impeding residual tumor eradication and fostering a permissive niche for recurrence. To decisively address this fundamental limitation and harness the potential of ablation to stimulate antitumor immunity, we proposed a nanotherapeutic immunomodulatory strategy that synchronously reversed postablation MDSC-driven immunosuppression ("release the immunosuppressive brakes") while activating the stimulator of interferon gene (STING) pathway-mediated antitumor immune priming ("apply the immunostimulatory accelerator") in the systemic immune landscape. Through rational design, we engineered the nanotherapeutic immunomodulators (termed cA@NPs, where NPs are nanoparticles) coencapsulating the STING agonist 2',3'-cyclic guanosine adenosine monophosphate (cGAMP) and the MDSC-differentiating agent all-trans retinoic acid (ATRA), effectively overcoming their disparate pharmacokinetic profiles while ensuring spatiotemporally coordinated delivery. The residual tumor models provided definitive evidence that reversing postablation MDSC-driven immunosuppression was essential for achieving more effective antitumor immunity. Comprehensive preclinical evaluations further demonstrated the cA@NPs' robust capacity to suppress micrometastasis, distant tumors, and orthotopic lesions via multidimensional remodeling of the postablation immune landscape. These findings established a mechanistic foundation for the clinical translation of ablation-synergized nanotherapy, effectively bridging localized thermal intervention with systemic immune potentiation to address tumor recurrence.

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Publication Details

Journal
ACS Nano
Published
2026-03-04
DOI
https://doi.org/10.1021/acsnano.5c10858
Primary Topic
Nanoplatforms for cancer theranostics
Type
article
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article

Reprogramming Postablation Tumor Immune Microenvironment with Dual-Function Nanotherapeutic Immunomodulator for Synergistic Antitumor Immunity and Recurrence Suppression

B Wang, Zhicheng Yan, Wenbo Wang, Bing He et al.
ACS Nano
Nanoplatforms for cancer theranostics
article

Reprogramming Postablation Tumor Immune Microenvironment with Dual-Function Nanotherapeutic Immunomodulator for Synergistic Antitumor Immunity and Recurrence Suppression

B Wang, Zhicheng Yan, Wenbo Wang, Bing He, Yuhan Shen, S Fan, Qiang Zhang, Hao Wu, Wei Yang, Song Wang
article en

Abstract

Radiofrequency ablation (RFA) has emerged as a predominant minimally invasive approach for liver tumors, achieving favorable therapeutic outcomes and triggering a systemic immune response via the release of tumor-associated antigens. However, postablation tumor recurrence remains a critical challenge in clinics. Our previous studies revealed that ablation-induced immunosuppression, primarily characterized by the expansion and activation of myeloid-derived suppressor cells (MDSCs), critically compromised the host's antitumor immunity, impeding residual tumor eradication and fostering a permissive niche for recurrence. To decisively address this fundamental limitation and harness the potential of ablation to stimulate antitumor immunity, we proposed a nanotherapeutic immunomodulatory strategy that synchronously reversed postablation MDSC-driven immunosuppression ("release the immunosuppressive brakes") while activating the stimulator of interferon gene (STING) pathway-mediated antitumor immune priming ("apply the immunostimulatory accelerator") in the systemic immune landscape. Through rational design, we engineered the nanotherapeutic immunomodulators (termed cA@NPs, where NPs are nanoparticles) coencapsulating the STING agonist 2',3'-cyclic guanosine adenosine monophosphate (cGAMP) and the MDSC-differentiating agent all-trans retinoic acid (ATRA), effectively overcoming their disparate pharmacokinetic profiles while ensuring spatiotemporally coordinated delivery. The residual tumor models provided definitive evidence that reversing postablation MDSC-driven immunosuppression was essential for achieving more effective antitumor immunity. Comprehensive preclinical evaluations further demonstrated the cA@NPs' robust capacity to suppress micrometastasis, distant tumors, and orthotopic lesions via multidimensional remodeling of the postablation immune landscape. These findings established a mechanistic foundation for the clinical translation of ablation-synergized nanotherapy, effectively bridging localized thermal intervention with systemic immune potentiation to address tumor recurrence.

ACS NanoVol. 20(10)
King University (US), Peking University (CN), Kindeva Drug Delivery (United States) (US), Ministry of Education (ET), State Key Laboratory of Natural and Biomimetic Drugs (CN)
Zero hunger, Good health and well-being
Openalex Percentile: Top 36%
Nanoplatforms for cancer theranostics
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