Evidence map›Paper›PMID 41377018›Full record

ArticleResearch (Washington, D.C.)2025

A DNA Nanomachine Modulates the Stemness-Associated Signaling Pathways for Overcoming Chemoresistance by Temporally Programming Drug Release.

Jie Chen, Xiaodie Li, Qian Chen, Xuyang Zhou, Jialin Zeng, Linlang Guo, Yinan Zhang, Dayong Yang, Chao Zhang

Abstract read
In one paragraph

Article in Research (Washington, D.C.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

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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

9 authors.

Jie ChenDepartment of Oncology, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, P. R. China.
Xiaodie LiDepartment of Oncology, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, P. R. China.
Qian ChenDepartment of Pathology, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, P. R. China.
Xuyang ZhouDepartment of Pathology, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, P. R. China.
Jialin ZengDepartment of Oncology, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, P. R. China.
Linlang GuoDepartment of Pathology, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, P. R. China.
Yinan ZhangSchool of Chemical Science and Engineering, Tongji University, Shanghai 200092, P. R. China.
Dayong YangDepartment of Chemistry, State Key Laboratory of Molecular Engineering of Polymers, Shanghai Key Laboratory of Molecular Catalysis and Innovative Materials, College of Chemistry and Materials, Fudan University, Shanghai 200438, P. R. China.
Chao ZhangDepartment of Oncology, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, P. R. China.ORCID https://orcid.org/0009-0007-8405-2164

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemoresistance is a primary cause of cancer treatment failure, due to the lack of specific regulatory strategies arising from unclear mechanisms. Here, we uncover the pivotal role of the PRMT1/SOX2 axis in regulating cancer stemness, a key factor contributing to cancer chemoresistance. In light of this, we construct a DNA nanomachine (DNM) to overcome chemoresistance by reversing cancer stemness. This DNM is constructed using a programmable DNA origami framework, incorporating CD44-targeting aptamers and glutathione (GSH)-responsive stemness inhibitors (DCLX069) as functional components. The DNM exhibits a specific affinity toward CD44-overexpressing tumor cells, enabling the effective delivery of the loaded cisplatin (CDDP) to the tumor cells. Upon entering the tumor cells, DCLX069 is rapidly released from the DNM due to high intracellular GSH levels, leading to swift regulation of the PRMT1/SOX2 axis. In contrast, CDDP exhibits a gradual enzymatic release profile. This temporally programmed release enables the reversal of cancer stemness before chemotherapy initiation, resulting in a substantial improvement in CDDP chemosensitivity and a significant increase in the median survival of tumor-bearing mice from 27 to over 56 d with DNM assistance. This study highlights the promising potential of this DNA nanotechnology-empowered therapy in addressing chemoresistance in malignant tumors.

Identifiers

PMID41377018
PMCPMC12687658

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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.