Evidence map›Paper›PMID 26138562›Full record

ArticleCancer gene therapy2015

Dual silencing of Bcl-2 and Survivin by HSV-1 vector shows better antitumor efficacy in higher PKR phosphorylation tumor cells in vitro and in vivo.

X Chen, Y Zhou, J Wang, J Wang, J Yang, Y Zhai, B Li

Abstract read
PubMed Publisher
In one paragraph

Article in Cancer gene therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

8 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Optimal delivery of RNA interference by viral vectors for cancer therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Review
  3. Review
  4. Article
  5. Virus-inspired strategies for cancer therapy.Seminars in cancer biology · 2022
    Review
  6. Review
  7. Article
  8. 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

7 authors at 2 institutions in 1 country.

X Chen1] OrienGene Biotechnology Ltd, Beijing, P.R.China [2] Key Laboratory for Cell Proliferation and Regulation Biology of State Education Ministry, College of Life Sciences, Beijing Normal University, Beijing, P.R.China.
Y Zhou1] SinoGenoMax Co., Ltd./Chinese National Human Genome Center, Beijing, P.R.China [2] Beijing Key Lab of Genomics, Beijing, P.R.China.
J WangOrienGene Biotechnology Ltd, Beijing, P.R.China.
J WangKey Laboratory for Cell Proliferation and Regulation Biology of State Education Ministry, College of Life Sciences, Beijing Normal University, Beijing, P.R.China.
J YangKey Laboratory for Cell Proliferation and Regulation Biology of State Education Ministry, College of Life Sciences, Beijing Normal University, Beijing, P.R.China.
Y ZhaiKey Laboratory for Cell Proliferation and Regulation Biology of State Education Ministry, College of Life Sciences, Beijing Normal University, Beijing, P.R.China.
B Li1] Key Laboratory for Cell Proliferation and Regulation Biology of State Education Ministry, College of Life Sciences, Beijing Normal University, Beijing, P.R.China [2] SinoGenoMax Co., Ltd./Chinese National Human Genome Center, Beijing, P.R.China [3] Beijing Key Lab of Genomics, Beijing, P.R.China.
Beijing Normal University · CNChinese National Human Genome Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

RNA interference (RNAi) is a promising tool for cancer therapy, but its delivery strategy is a major challenge for its application. Oncolytic herpes simplex virus type 1 (HSV-1) is not only an effective antitumor drug but also an excellent vector. Herein, RNAi of oncogenes Bcl-2 and Survivin was combined with oncolytic HSV-1 (ICP34.5-/ICP6-/ICP47-/CMV-GM-CSF) and a new vector HSV010-BS was constructed. Transfected cell viability assays and animal experiments revealed that the dual silencing of Bcl-2 and Survivin improved the antitumor effect of oncolytic HSV-1 in vitro and in vivo, while the antitumor effect was correlated with the phosphorylation levels of PKR of the tumor cells. The higher the phosphorylation levels of PKR of the tumor cells, the weaker the replication ability of oncolytic HSV-1, and the more powerful HSV010-BS was than its control vectors in inhibiting the growth of the tumor cells. The results provided direct supportive proofs for a new potential cancer therapy strategy.

Indexed as

AnimalsAntineoplastic AgentsCell Line, TumoreIF-2 KinaseFemaleGene Knockdown TechniquesGenetic TherapyGenetic VectorsHerpesvirus 1, HumanHumansInhibitor of Apoptosis ProteinsMice, NudeMolecular Targeted TherapyOncolytic VirotherapyPhosphorylationProto-Oncogene Proteins c-bcl-2Antineoplastic AgentsBIRC5 protein, humaneIF-2 KinaseInhibitor of Apoptosis ProteinsProto-Oncogene Proteins c-bcl-2Survivin

Identifiers

PMID26138562
OpenAlexW1596000484

What OpenQuestion holds

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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.