Evidence map›Paper›PMID 35988145›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2022

Versatile Nano-PROTAC-Induced Epigenetic Reader Degradation for Efficient Lung Cancer Therapy.

Huan-Tian Zhang, Rui Peng, Sheng Chen, Ao Shen, Lixin Zhao, Wang Tang, Xiao-He Wang, Zhen-Yan Li, Zhen-Gang Zha, Mengmeng Yi and 1 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing 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

53 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Programmed cell death in lung cancer: mechanisms, immune responses, and therapeutics.Apoptosis : an international journal on programmed cell death · 2026
    Review
  8. Article
  9. Review
  10. Dynamic reprogramming of the tumor immune network via multicycle checkpoint degradation for cancer immunotherapy.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  11. Article
  12. Review
  13. Targeted Inhibition of CD74Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article
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

11 authors.

Huan-Tian ZhangDepartment of Bone and Joint Surgery, the First Affiliated Hospital, Jinan University, Guangzhou, Guangdong, 510630, P. R. China.
Rui PengDepartment of Bone and Joint Surgery, the First Affiliated Hospital, Jinan University, Guangzhou, Guangdong, 510630, P. R. China.
Sheng ChenDepartment of Bone and Joint Surgery, the First Affiliated Hospital, Jinan University, Guangzhou, Guangdong, 510630, P. R. China.
Ao ShenKey Laboratory of Molecular Target & Clinical Pharmacology and the State & NMPA Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences & The Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 511436, P. R. China.
Lixin ZhaoKey Laboratory of Molecular Target & Clinical Pharmacology and the State & NMPA Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences & The Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 511436, P. R. China.
Wang TangDepartment of Bone and Joint Surgery, the First Affiliated Hospital, Jinan University, Guangzhou, Guangdong, 510630, P. R. China.
Xiao-He WangDepartment of Bone and Joint Surgery, the First Affiliated Hospital, Jinan University, Guangzhou, Guangdong, 510630, P. R. China.
Zhen-Yan LiDepartment of Bone and Joint Surgery, the First Affiliated Hospital, Jinan University, Guangzhou, Guangdong, 510630, P. R. China.
Zhen-Gang ZhaDepartment of Bone and Joint Surgery, the First Affiliated Hospital, Jinan University, Guangzhou, Guangdong, 510630, P. R. China.
Mengmeng YiKey Laboratory of Molecular Target & Clinical Pharmacology and the State & NMPA Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences & The Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 511436, P. R. China.
Lingmin ZhangDepartment of Bone and Joint Surgery, the First Affiliated Hospital, Jinan University, Guangzhou, Guangdong, 510630, P. R. China.ORCID 0000-0002-4215-5401

Funding

Guangzhou Science and Technology Project 201707010493Guangzhou Science and Technology Project 202102010069Macau Foundation for Development of Science and Technology 0029/2019/ANational Natural Science Foundation of China 81602360National Natural Science Foundation of China 81672224National Natural Science Foundation of China 81700382National Natural Science Foundation of China 81871809National Natural Science Foundation of China 82072470Natural Science Foundation of Guangdong Province 2017A030313665Natural Science Foundation of Guangdong Province 2019A1515011082Natural Science Foundation of Guangdong Province 2019A1515012166Natural Science Foundation of Guangdong Province 2021A1515012154Youth Talent Support Project of Guangzhou Association for Science & Technology X20200301018
6 · The paper itself

Abstract

Recent evidence has indicated that overexpression of the epigenetic reader bromodomain-containing protein 4 (BRD4) contributes to a poor prognosis of lung cancers, and the suppression of its expression promotes cell apoptosis and leads to tumor shrinkage. Proteolysis targeting chimera (PROTAC) has recently emerged as a promising therapeutic strategy with the capability to precisely degrade targeted proteins. Herein, a novel style of versatile nano-PROTAC (CREATE (CRV-LLC membrane/DS-PLGA/dBET6)) is developed, which is constructed by using a pH/GSH (glutathione)-responsive polymer (disulfide bond-linked poly(lactic-co-glycolic acid), DS-PLGA) to load BRD4-targeted PROTAC (dBET6), followed by the camouflage with engineered lung cancer cell membranes with dual targeting capability. Notably, CREATE remarkably confers simultaneous targeting ability to lung cancer cells and tumor-associated macrophages (TAMs). The pH/GSH-responsive design improves the release of dBET6 payload from nanoparticles to induce pronounced apoptosis of both cells, which synergistically inhibits tumor growth in both subcutaneous and orthotopic tumor-bearing mouse model. Furthermore, the efficient tumor inhibition is due to the direct elimination of lung cancer cells and TAMs, which remodels the tumor microenvironment. Taken together, the results elucidate the construction of a versatile nano-PROTAC enables to eliminate both lung cancer cells and TAMs, which opens a new avenue for efficient lung cancer therapy via PROTAC.

Indexed as

Lung NeoplasmsTranscription FactorsAnimalsDisulfidesEpigenesis, GeneticGlutathioneMiceNuclear ProteinsPolylactic Acid-Polyglycolic Acid CopolymerPolymersProteolysisTumor MicroenvironmentDisulfidesGlutathioneNuclear ProteinsPolylactic Acid-Polyglycolic Acid CopolymerPolymersTranscription FactorsBRD4epigenetic readerPROTACtumor-associated macrophagestumor microenvironment

Identifiers

PMID35988145
PMCPMC9561860

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Registered trials

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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.