Evidence map›Paper›PMID 38557176›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2024

Development of an aptamer capable of multidrug resistance reversal for tumor combination chemotherapy.

Xiaohong Wen, Zhixiang Huang, Xiaohai Yang, Xiaoxiao He, Lie Li, Haiyan Chen, Kemin Wang, Qiuping Guo, Jianbo Liu

Open access · hybridAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
4.4field-weighted citation impact, top 5% of its field
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

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Identifying a cancer therapeutic target: Cell-SELEX identifies a membrane protein for aptamer-mediated growth suppression.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Advances in aptamer technology for target-based drug discovery.Journal of pharmaceutical analysis · 2026
    Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. 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

9 authors at 1 institution in 1 country.

Xiaohong WenState Key Laboratory of Chemo/Biosensing and Chemometrics, Hunan University, Changsha 410082, China.
Zhixiang HuangState Key Laboratory of Chemo/Biosensing and Chemometrics, Hunan University, Changsha 410082, China.
Xiaohai YangState Key Laboratory of Chemo/Biosensing and Chemometrics, Hunan University, Changsha 410082, China.
Xiaoxiao HeState Key Laboratory of Chemo/Biosensing and Chemometrics, Hunan University, Changsha 410082, China.
Lie LiState Key Laboratory of Chemo/Biosensing and Chemometrics, Hunan University, Changsha 410082, China.
Haiyan ChenState Key Laboratory of Chemo/Biosensing and Chemometrics, Hunan University, Changsha 410082, China.
Kemin WangState Key Laboratory of Chemo/Biosensing and Chemometrics, Hunan University, Changsha 410082, China.
Qiuping GuoState Key Laboratory of Chemo/Biosensing and Chemometrics, Hunan University, Changsha 410082, China.
Jianbo LiuState Key Laboratory of Chemo/Biosensing and Chemometrics, Hunan University, Changsha 410082, China.ORCID 0000-0001-8282-4078
Hunan University · CN

Funding

Foundation for Innovative Research Groups of the National Natural Science Foundation of China 21521063Foundation for Innovative Research Groups of the National Natural Science Foundation of China 21735002Foundation for Innovative Research Groups of the National Natural Science Foundation of China 21877030Foundation for Innovative Research Groups of the National Natural Science Foundation of China 22177032Foundation for Innovative Research Groups of the National Natural Science Foundation of China 22377025
6 · The paper itself

Abstract

Multidrug resistance (MDR) is a major factor in the failure of many forms of tumor chemotherapy. Development of a specific ligand for MDR-reversal would enhance the intracellular accumulation of therapeutic agents and effectively improve the tumor treatments. Here, an aptamer was screened against a doxorubicin (DOX)-resistant human hepatocellular carcinoma cell line (HepG2/DOX) via cell-based systematic evolution of ligands by exponential enrichment. A 50 nt truncated sequence termed d3 was obtained with high affinity and specificity for HepG2/DOX cells. Multidrug resistance protein 1 (MDR1) is determined to be a possible recognition target of the selected aptamer. Aptamer d3 binding was revealed to block the MDR of the tumor cells and increase the accumulation of intracellular anticancer drugs, including DOX, vincristine, and paclitaxel, which led to a boost to the cell killing of the anticancer drugs and lowering their survival of the tumor cells. The aptamer d3-mediated MDR-reversal for effective chemotherapy was further verified in an in vivo animal model, and combination of aptamer d3 with DOX significantly improved the suppression of tumor growth by treating a xenograft HepG2/DOX tumor in vivo. This work demonstrates the feasibility of a therapeutic DNA aptamer as a tumor MDR-reversal agent, and combination of the selected aptamer with chemotherapeutic drugs shows great potential for liver cancer treatments.

Indexed as

Antineoplastic AgentsDrug Resistance, NeoplasmAnimalsCell Line, TumorDoxorubicinDrug Resistance, MultipleDrug Therapy, CombinationHumansAntineoplastic AgentsDoxorubicinDNA aptamerhepatocellular carcinomaMDR-reversalmultidrug resistancetumor combination chemotherapy

Identifiers

PMID38557176
PMCPMC11009676
OpenAlexW4393380905

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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 OpenQuestion graph.