Evidence map›Paper›PMID 40230650›Full record

ArticleMaterials today. Bio2025

Construction of a programmed activation nanosystem based on intracellular hypoxia in cisplatin-resistant tumor cells for reversing cisplatin resistance.

Yurong Liu, Longqing Si, Yunheng Liu, Song Li, Xiaokang Zhang, Shaojing Jiang, Wenjing Liu, Xiaolin Li, Lianguo Zhang, Hongxia Zheng and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Materials today. Bio, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

13 authors.

Yurong LiuSchool of Pharmacy, Binzhou Medical University, Yantai, 264003, China.
Longqing SiSchool of Pharmacy, Binzhou Medical University, Yantai, 264003, China.
Yunheng LiuSchool of Pharmacy, Binzhou Medical University, Yantai, 264003, China.
Song LiSchool of Pharmacy, Binzhou Medical University, Yantai, 264003, China.
Xiaokang ZhangSchool of Pharmacy, Binzhou Medical University, Yantai, 264003, China.
Shaojing JiangYantai Engineering Research Center for Digital Technology of Stomatology, School of Stomatology, Binzhou Medical University, Yantai, 264003, China.
Wenjing LiuSchool of Pharmacy, Binzhou Medical University, Yantai, 264003, China.
Xiaolin LiSchool of Pharmacy, Binzhou Medical University, Yantai, 264003, China.
Lianguo ZhangDepartment of Thoracic Surgery, Binzhou Medical University Hospital, Binzhou, 256603, China.
Hongxia ZhengSchool of Pharmacy, Binzhou Medical University, Yantai, 264003, China.
Zhonghao LiuYantai Engineering Research Center for Digital Technology of Stomatology, School of Stomatology, Binzhou Medical University, Yantai, 264003, China.
Jinghui HuYantai Engineering Research Center for Digital Technology of Stomatology, School of Stomatology, Binzhou Medical University, Yantai, 264003, China.
Jing ChenSchool of Pharmacy, Binzhou Medical University, Yantai, 264003, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer poses a significant threat to human life and health. Cancers treated with cisplatin invariably develop drug resistance. This challenge can be overcome by identifying and exploiting the vulnerabilities acquired by drug-resistant cancer cells, paving the way for finding effective novel treatment options for cisplatin-resistant cancers. Our previous study revealed that cisplatin resistance in cancer cells comes at the cost of increased intracellular hypoxia. In this study, we used 2-nitroimidazole modified hyaluronic acid (HA-NI) as the carrier. The cisplatin-resistant tumor cell specific intracellular hypoxia programmed activation nanomedicine (T/C@HN NPs) was constructed by the hypoxic toxic drug tirapazamine (TPZ) and encapsulating chlorin e6 (Ce6) into HA-NI using polymer assembly technology. The amphiphilic carrier could release free Ce6 molecules under the stimulation of intracellular hypoxic environment, and exhibit specific "activated state" photodynamic properties in cisplatin-resistant tumor cells. Upon irradiation, Ce6-mediated photodynamic therapy further intensifies hypoxia, amplifying its cytotoxicity. This project systematically evaluated the effects of T/C@HN NPs on the identification and recognition of cisplatin-resistant tumors using drug-resistant patient-derived xenograft (PDX) models. This study provides a promising avenue for the development of novel treatment of cisplatin-resistant tumors.

Indexed as

Cisplatin-resistantHypoxia activationIntracellular hypoxiaNanomedicineProgram activation

Identifiers

PMID40230650
PMCPMC11995088

What Socratic holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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 Socratic graph.