Evidence map›Paper›PMID 41611660›Full record

ArticleSignal transduction and targeted therapy2026

Employing epigenetic protein degradation techniques to block CCL5-mediated photodynamic therapy via a programmed delivery platform.

Tingting Yang, Yuzhu Hu, Anjie Guo, Xifeng Zhang, Wanyu Wang, Linbin Yi, Rui Zhang, Xinyu Gou, Zhiyong Qian, Bilan Wang and 2 more

Abstract read
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In one paragraph

Article in Signal transduction and targeted therapy, 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
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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

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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

12 authors.

Tingting YangDepartment of Neurosurgery and Institute of Neurosurgery, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, West China Medical School, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, China.
Yuzhu HuDepartment of Neurosurgery and Institute of Neurosurgery, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, West China Medical School, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, China.
Anjie GuoDepartment of Neurosurgery and Institute of Neurosurgery, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, West China Medical School, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, China.
Xifeng ZhangDepartment of Neurosurgery and Institute of Neurosurgery, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, West China Medical School, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, China.
Wanyu WangDepartment of Neurosurgery and Institute of Neurosurgery, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, West China Medical School, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, China.
Linbin YiDepartment of Neurosurgery and Institute of Neurosurgery, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, West China Medical School, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, China.
Rui ZhangDepartment of Neurosurgery and Institute of Neurosurgery, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, West China Medical School, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, China.
Xinyu GouDepartment of Neurosurgery and Institute of Neurosurgery, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, West China Medical School, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, China.
Zhiyong QianDepartment of Neurosurgery and Institute of Neurosurgery, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, West China Medical School, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, China.
Bilan WangDepartment of Pharmacy, West China Second University Hospital of Sichuan University, Chengdu, PR China. bilan@scu.edu.cn.
Yongzhong ChengDepartment of Neurosurgery and Institute of Neurosurgery, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, West China Medical School, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, China. chengyz@scu.edu.cn.
Xiang GaoDepartment of Neurosurgery and Institute of Neurosurgery, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, West China Medical School, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, China. xianggao@scu.edu.cn.ORCID http://orcid.org/0000-0001-7478-5072

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32222046 and 82172630
6 · The paper itself

Abstract

Despite the significant potential of photodynamic therapy (PDT) in cancer treatment, further refinement is needed to address challenges such as poor tumor-specific accumulation of photosensitizers and the development of therapeutic resistance, which may be regulated by epigenetics. Here, a novel tumor microenvironment-responsive delivery platform was developed to co-deliver epigenetic protein degraders and photosensitizers, aiming to block the relevant regulatory mechanisms and enhance the effectiveness of combination therapy. Benefiting from the targeting ability, pH-triggered charge reversal, and intracellular glutathione (GSH)-responsive release, the delivery platform exhibited enhanced tumor accumulation and therapeutic effects. The mechanism of action revealed that the precise accumulation and release of drugs via the tumor-orchestrated delivery system not only regulated cell growth and immune activation, but also inhibited the expression of tumor immune escape molecules (PDL1 and CD47) and M2 macrophage polarization, significantly increasing the anti-breast cancer and anti-melanoma effects of PDT in the presence of an epigenetic modifier. More importantly, we found for the first time that photodynamic therapy can generate therapeutic resistance through the upregulation of CCL5, and confirmed that this resistance can be reduced by the epigenetic degradation of bromodomain-containing protein 4 (BRD4). These findings underscore the potential of integrating PDT with epigenetic protein degraders through a programmed delivery platform, offering a promising strategy for improving cancer treatment outcomes.

Indexed as

Chemokine CCL5Epigenesis, GeneticPhotochemotherapyPhotosensitizing AgentsAnimalsCell Line, TumorFemaleHumansMiceProteolysisTumor MicroenvironmentChemokine CCL5Photosensitizing Agents

Identifiers

PMID41611660
PMCPMC12855822

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.