Evidence map›Paper›PMID 41732379›Full record

ArticleMaterials today. Bio2026

A versatile nanoplatform for enhancing the therapeutic efficacy against low-immunogenic TNBC by inducing immunogenic cell death and MHC-I upregulation.

Shanlingzi Huang, Lu Gao, Yujun Chen, Zhaoming Fu, Ziyou Wang, Yifan Liu, Zhicheng Zhou, Ru Huang, Wen Song, Feifan Zhou

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Materials today. Bio, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Shanlingzi HuangState Key Laboratory of Digital Medical Engineering, School of Biomedical Engineering, Hainan University, Sanya, 572025, China.
Lu GaoState Key Laboratory of Digital Medical Engineering, School of Biomedical Engineering, Hainan University, Sanya, 572025, China.
Yujun ChenState Key Laboratory of Digital Medical Engineering, School of Biomedical Engineering, Hainan University, Sanya, 572025, China.
Zhaoming FuState Key Laboratory of Digital Medical Engineering, School of Biomedical Engineering, Hainan University, Sanya, 572025, China.
Ziyou WangState Key Laboratory of Digital Medical Engineering, School of Biomedical Engineering, Hainan University, Sanya, 572025, China.
Yifan LiuState Key Laboratory of Digital Medical Engineering, School of Biomedical Engineering, Hainan University, Sanya, 572025, China.
Zhicheng ZhouState Key Laboratory of Digital Medical Engineering, School of Biomedical Engineering, Hainan University, Sanya, 572025, China.
Ru HuangState Key Laboratory of Digital Medical Engineering, School of Biomedical Engineering, Hainan University, Sanya, 572025, China.
Wen SongState Key Laboratory of Digital Medical Engineering, School of Biomedical Engineering, Hainan University, Sanya, 572025, China.
Feifan ZhouState Key Laboratory of Digital Medical Engineering, School of Biomedical Engineering, Hainan University, Sanya, 572025, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC), characterized by low immunogenicity, is a challenging issue in clinical treatment due to its poor response to various therapies. The transformation of TNBC from a "cold tumor" with low immunogenicity into a "hot tumor" that elicits stronger immune responses is a key research focus. Photodynamic therapy (PDT) has emerged as a promising solution for TNBC treatment because it can effectively induce immunogenic cell death (ICD), which prompts the release of damage-associated molecular patterns (DAMPs) and activates immune responses. The role of MHC-I molecules in antigen presentation is crucial, but TNBC cells often evade immune surveillance by downregulating or losing MHC-I expression. Recent studies have shown that inhibiting the activity of complex II (CII) in the mitochondrial electron transport chain of tumor cells can promote MHC-I expression. Based on this finding, the combination of the PDT photosensitizer PCN-224 with the CII inhibitor 3-nitropropionic acid (3NPA) to form PCN@3NPA has been innovatively developed. Furthermore, modification with hyaluronic acid (HA) enables targeted delivery to TNBC cells that overexpress CD44. PDT induces ICD in tumor cells, releasing large amounts of DAMPs, while the sustained release of 3NPA effectively inhibits CII activity, significantly enhances MHC-I expression, thereby boosting tumor cell immunogenicity. This process significantly improves the recognition and killing of tumor cells by CD8

Indexed as

Antigen presentationLow immunogenicityMHC-I upregulationMitochondrial electron transport chainPhotodynamic therapy

Identifiers

PMID41732379
PMCPMC12925286

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