Evidence map›Paper›PMID 22509396›Full record

ArticlePloS one2012

Prostate cancer-specific and potent antitumor effect of a DD3-controlled oncolytic virus harboring the PTEN gene.

Miao Ding, Xin Cao, Hai-neng Xu, Jun-kai Fan, Hong-ling Huang, Dong-qin Yang, Yu-hua Li, Jian Wang, Runsheng Li, Xin-yuan Liu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Article
  3. Oncolyic Virotherapy for Prostate Cancer: Lighting a Fire in Winter.International journal of molecular sciences · 2022
    Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Oncolytic virotherapy for urological cancers.Nature reviews. Urology · 2016
    Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. 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

10 authors at 5 institutions in 2 countries.

Miao DingState Key Laboratory of Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Xin Cao
Hai-neng Xu
Jun-kai Fan
Hong-ling Huang
Dong-qin Yang
Yu-hua Li
Jian Wang
Runsheng Li
Xin-yuan Liu
Chinese Academy of Sciences · CNShanghai Institute of Planned Parenthood Research · CNCenter for Excellence in Molecular Cell Science · CNShanghai Institutes for Biological Sciences · CNUniversity of Kentucky · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer is a major health problem for men in Western societies. Here we report a Prostate Cancer-Specific Targeting Gene-Viro-Therapy (CTGVT-PCa), in which PTEN was inserted into a DD3-controlled oncolytic viral vector (OV) to form Ad.DD3.E1A.E1B(Δ55)-(PTEN) or, briefly, Ad.DD3.D55-PTEN. The woodchuck post-transcriptional element (WPRE) was also introduced at the downstream of the E1A coding sequence, resulting in much higher expression of the E1A gene. DD3 is one of the most prostate cancer-specific genes and has been used as a clinical bio-diagnostic marker. PTEN is frequently inactivated in primary prostate cancers, which is crucial for prostate cancer progression. Therefore, the Ad.DD3.D55-PTEN has prostate cancer specific and potent antitumor effect. The tumor growth rate was almost completely inhibited with the final tumor volume after Ad.DD3.D55-PTEN treatment less than the initial volume at the beginning of Ad.DD3.D55-PTEN treatment, which shows the powerful antitumor effect of Ad.DD3.D55-PTEN on prostate cancer tumor growth. The CTGVT-PCa construct reported here killed all of the prostate cancer cell lines tested, such as DU145, 22RV1 and CL1, but had a reduced or no killing effect on all the non-prostate cancer cell lines tested. The mechanism of action of Ad.DD3.D55-PTEN was due to the induction of apoptosis, as detected by TUNEL assays and flow cytometry. The apoptosis was mediated by mitochondria-dependent and -independent pathways, as determined by caspase assays and mitochondrial membrane potential.

Indexed as

Adenovirus E1A ProteinsAnimalsAntigens, NeoplasmApoptosisCell Line, TumorGenetic TherapyGenetic VectorsHumansMaleMiceMice, NudeOncolytic VirotherapyOncolytic VirusesProstatic NeoplasmsPTEN PhosphohydrolaseAdenovirus E1A ProteinsAntigens, Neoplasmprostate cancer antigen 3, humanPTEN PhosphohydrolasePTEN protein, human

Identifiers

PMID22509396
PMCPMC3324420
OpenAlexW2121028233

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.