Evidence map›Paper›PMID 30594071›Full record

ArticleMolecular therapy. Nucleic acids2019

An RNA Aptamer Targeting the Receptor Tyrosine Kinase PDGFRα Induces Anti-tumor Effects through STAT3 and p53 in Glioblastoma.

Sorah Yoon, Xiwei Wu, Brian Armstrong, Nagy Habib, John J Rossi

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy. Nucleic acids, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.1field-weighted citation impact, top 10% 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

37 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Using aptamers for targeted delivery of RNA therapies.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Aptamer-Based Tumor-Targeted Diagnosis and Drug Delivery.Advances in experimental medicine and biology · 2023
    Review
  18. Roles of STAT3 in the pathogenesis and treatment of glioblastoma.Frontiers in cell and developmental biology · 2023
    Review
  19. Therapeutic Potential of Aptamer-Protein Interactions.ACS pharmacology & translational science · 2022
    Review
  20. JMJD family proteins in cancer and inflammation.Signal transduction and targeted therapy · 2022
    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

5 authors at 3 institutions in 2 countries.

Sorah YoonDepartment of Molecular and Cellular Biology, Beckman Research Institute of City of Hope, Duarte, CA 91010, USA.
Xiwei WuIntegrative Genomic Core, City of Hope, Duarte, CA 91010, USA.
Brian ArmstrongLight Microscopy Core, City of Hope, Duarte, CA 91010, USA.
Nagy HabibDepartment of Surgery and Cancer, Imperial College London, London W12 0NN, UK.
John J RossiDepartment of Molecular and Cellular Biology, Beckman Research Institute of City of Hope, Duarte, CA 91010, USA; Irell and Manella Graduate School of Biological Sciences, Beckman Research Institute of City of Hope, Duarte, CA 91010, USA. Electronic address: jrossi@coh.org.
Beckman Research InstituteCity of Hope · USImperial College London · GB

Funding

Transgenic Mouse FacilityP30CA033572 · NCI · CITY OF HOPE/BECKMAN RESEARCH INSTITUTE · PI John Charles Williams · 1985 to 2026
$86.3M
COMBINATORIAL USE OF CCR5 RIBOZYMES WITH ANTI HIV1 RNASR01AI042552 · NIAID · CITY OF HOPE/BECKMAN RESEARCH INSTITUTE · PI ROSSI, JOHN JOSEPH · 1998 to 2019
$7.8M
NCI NIH HHS P30 CA033572NIAID NIH HHS R01 AI042552
6 · The paper itself

Abstract

Human glioblastoma (GBM) is the most aggressive malignancy of the CNS, with less than 5% survival. Despite great efforts to find effective therapeutics, current options remain very limited. To develop a targeted cancer therapeutic, we selected RNA aptamers against platelet-derived growth factor receptor α (PDGFRα), which is a receptor tyrosine kinase. One RNA aptamer (PDR3) with high affinity (0.25 nM) showed PDGFRα specificity and was internalized in U251-MG cells. Following treatment with the PDR3 aptamer, expression of the transcription factor STAT3 (signal transducer and activator of transcription 3) was inhibited, whereas the expression of the histone demethylase JMJD3 and the tumor suppressor p53 were upregulated. PDR3 also upregulated serine phosphorylation of p53, which subsequently mediated apoptosis through the death receptors: tumor necrosis factor (TNF)-related apoptosis-inducing ligand receptors 1/2 (TRAIL-R1/R2), Fas-associated via death domain (FADD), and Fas. PDR3 significantly decreased cell viability in a dose-dependent manner. Furthermore, translocation of PDR3 into the nucleus induced hypomethylation at the promoters of cyclin D2. To assess the feasibility of targeted delivery, we conjugated PDR3 aptamer with STAT3-siRNA for a chimera. The PDR3-siSTAT3 chimera successfully inhibited the expression of target genes and showed significant inhibition of cell viability. In summary, our results show that well-tailored RNA aptamers targeting the PDGFRα-STAT3 axis have the potential to act as anti-cancer therapeutics in GBM.

Indexed as

apoptosisGBMp53PDGFRα aptamerSTAT3

Identifiers

PMID30594071
PMCPMC6307106
OpenAlexW2903387613

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.