Evidence map›Paper›PMID 27014974›Full record

ArticleOncotarget2016

Enhancing DPYSL3 gene expression via a promoter-targeted small activating RNA approach suppresses cancer cell motility and metastasis.

Changlin Li, Wencong Jiang, Qingting Hu, Long-Cheng Li, Liang Dong, Ruibao Chen, Yinghong Zhang, Yuzhe Tang, J Brantley Thrasher, Chang-Bai Liu and 1 more

Abstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed.

  1. Aptamers in cancer therapy: Why has clinical translation lagged behind preclinical promise?Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026
    Review
  2. Review
  3. Article
  4. Review
  5. Molecular therapy. Nucleic acids · 2023
    Article
  6. Review
  7. Article
  8. Review
  9. Approaches to Gene Modulation Therapy for ALS.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022
    Review
  10. Aptamers: Cutting edge of cancer therapies.Molecular therapy : the journal of the American Society of Gene Therapy · 2021
    Review
  11. Review
  12. Article
  13. Article
  14. Upregulation ofInternational journal of molecular sciences · 2020
    Article
  15. DPYSL3 modulates mitosis, migration, and epithelial-to-mesenchymal transition in claudin-low breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  16. Aptamer-iRNAs as Therapeutics for Cancer Treatment.Pharmaceuticals (Basel, Switzerland) · 2018
    Review
  17. Article
  18. Review
  19. Review
  20. 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

11 authors.

Changlin LiDepartment of Urology, University of Kansas Medical Center, Kansas City, KS 66160, USA.
Wencong JiangDepartment of Urology, University of Kansas Medical Center, Kansas City, KS 66160, USA.
Qingting HuDepartment of Urology, University of Kansas Medical Center, Kansas City, KS 66160, USA.
Long-Cheng LiLaboratory of Molecular Medicine, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100073, China.
Liang DongDepartment of Urology, University of Kansas Medical Center, Kansas City, KS 66160, USA.
Ruibao ChenDepartment of Urology, University of Kansas Medical Center, Kansas City, KS 66160, USA.
Yinghong ZhangDepartment of Urology, University of Kansas Medical Center, Kansas City, KS 66160, USA.
Yuzhe TangDepartment of Urology, University of Kansas Medical Center, Kansas City, KS 66160, USA.
J Brantley ThrasherDepartment of Urology, University of Kansas Medical Center, Kansas City, KS 66160, USA.
Chang-Bai LiuInstitute of Cell Therapy, China Three Gorges University, Yichang 443002, China.
Benyi LiDepartment of Urology, University of Kansas Medical Center, Kansas City, KS 66160, USA.

Funding

Prostate-targeted CRMP4 saRNA as anti-metastatic therapyR21CA175279 · NCI · UNIVERSITY OF KANSAS MEDICAL CENTER · PI LI, BENYI · 2014 to 2015
$361k
NCI NIH HHS R21 CA175279
6 · The paper itself

Abstract

To explore a novel strategy in suppressing tumor metastasis, we took the advantage of a recent RNA activation (RNAa) theory and used small double-strand RNA molecules, termed as small activating RNAs (saRNA) that are complimentary to target gene promoter, to enhance transcription of metastasis suppressor gene. The target gene in this study is Dihydro-pyrimidinase-like 3 (DPYSL3, protein name CRMP4), which was identified as a metastatic suppressor in prostate cancers. There are two transcriptional variants of DPYSL3 gene in human genome, of which the variant 2 is the dominant transcript (DPYSL3v2, CRMP4a) but is also significantly down-regulated in primary prostate cancers. A total of 8 saRNAs for DPYSL3v1 and 14 saRNAs for DPYSL3v2 were tested in multiple prostate cancer cell lines. While none of the saRNAs significantly altered DPYSL3v1 expression, 4 saRNAs showed a strong enhancing effect on DPYSL3v2 expression, resulting in reduced cell mobility in vitro. To achieve a prostate cancer-specific delivery for in vivo testing, we conjugated the most potent saV2-9 RNA molecule with the prostate-specific membrane antigen (PSMA)-targeting aptamer A10-3.2. The conjugates successful increased DPYSL3v2 gene expression in PSMA-positive but not PSMA-negative prostate cancer cells. In nude mice bearing orthotopic xenograft of prostate cancer, a 10-day consecutive treatment with the saV2-9 conjugates significantly suppress distal metastasis compared to the control saRNAs. Analysis of xenograft tissues revealed that DPYSL3v2 expression was largely increased in saV2-9 conjugate-treated group compared to the control group. In conclusion, DPYSL3v2 promoter-targeted saRNA molecules might be used as an adjunctive therapy to suppress prostate cancer metastasis.

Indexed as

AnimalsCell Line, TumorCell MovementGene ExpressionGenetic TherapyHeterograftsHumansMaleMiceMice, NudeMuscle ProteinsNeoplasm InvasivenessProstatic NeoplasmsProtein IsoformsRNA, Double-StrandedTranscriptional ActivationDPYSL3 protein, humanMuscle ProteinsProtein IsoformsRNA, Double-StrandedCRMP4DPYSL3metastasisRNAasaRNA

Identifiers

PMID27014974
PMCPMC5008410

What OpenQuestion holds

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LicenceCC BY
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 OpenQuestion graph.