Evidence map›Paper›PMID 26251031›Full record

ArticleCancer gene therapy2015

Expression of p53 synergistically augments caspases-mediated apoptosis induced by replication-competent adenoviruses in pancreatic carcinoma cells.

Y Takei, S Okamoto, K Kawamura, Y Jiang, T Morinaga, M Shingyoji, I Sekine, S Kubo, Y Tada, K Tatsumi and 4 more

Abstract readComparative Study
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 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 28% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

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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

14 authors at 6 institutions in 1 country.

Y TakeiDepartment of Molecular Cell Biology, Graduate School of Pharmaceutical Sciences, Chiba University, Chiba, Japan.
S OkamotoDivision of Pathology and Cell Therapy, Chiba Cancer Center Research Institute, Chiba, Japan.
K KawamuraDivision of Pathology and Cell Therapy, Chiba Cancer Center Research Institute, Chiba, Japan.
Y JiangDivision of Pathology and Cell Therapy, Chiba Cancer Center Research Institute, Chiba, Japan.
T MorinagaDepartment of Molecular Cell Biology, Graduate School of Pharmaceutical Sciences, Chiba University, Chiba, Japan.
M ShingyojiDivision of Respirology, Chiba Cancer Center, Chiba, Japan.
I SekineDepartment of Medical Oncology, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
S KuboDepartment of Genetics, Hyogo College of Medicine, Nishinomiya, Japan.
Y TadaDepartment of Respirology, Graduate School of Medicine, Chiba University, Chiba, Japan.
K TatsumiDepartment of Respirology, Graduate School of Medicine, Chiba University, Chiba, Japan.
H ShimadaDepartment of Surgery, School of Medicine, Toho University, Tokyo, Japan.ORCID http://orcid.org/0000-0002-1990-8217
K HiroshimaDepartment of Pathology, Tokyo Women's Medical University Yachiyo Medical Center, Yachiyo, Japan.
N YamaguchiDepartment of Molecular Cell Biology, Graduate School of Pharmaceutical Sciences, Chiba University, Chiba, Japan.
M TagawaDivision of Pathology and Cell Therapy, Chiba Cancer Center Research Institute, Chiba, Japan.
Chiba University · JPChiba Cancer Center · JPHyogo Medical University · JPToho University · JPTokyo Women's Medical University · JPUniversity of Tsukuba · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We examined cytotoxicity of replication-competent type 5 adenoviruses (Ad5) in human pancreatic carcinoma cells with a p53-defective genotype. The replication-competent Ad5 of which E1A gene was activated by exogenous transcriptional regulatory sequences, derived from the midkine and survivin genes, achieved cytotoxicity to the pancreatic carcinoma. These cells were susceptible to replication-incompetent Ad5 expressing the wild-type p53 gene. We also produced the replication-competent Ad5 bearing the same exogenous regulatory sequences and the type 35 Ad-derived fiber-knob region, and showed that the cytotoxicity was comparable to that of the replication-competent Ad5 prototype. We then investigated possible combinatory effects of the fiber-modified replication-competent Ad and Ad5 expressing the wild-type p53 gene, both of which did not interfere respective infections. The combination produced synergistic cytotoxic effects with enhanced cleavages of caspase-3 and PARP molecules, and with increased sub-G1 fractions and annexin V-positive populations although the viral production of the replication-competent Ad was rather suppressed by expressed p53. Pancreatic cells infected with both Ad showed increase of p53 and decrease of MDM2 and p21 levels, compared with those infected with Ad expressing the p53 gene. These data collectively indicated that replication-competent Ad augmented susceptibility of pancreatic cells to apoptosis through upregulated p53 expression.

Indexed as

AdenocarcinomaAdenovirus E1A ProteinsAdenoviruses, HumanApoptosisCapsid ProteinsCaspase 3Cell CycleCell Line, TumorCyclin-Dependent Kinase Inhibitor p21Cytopathogenic Effect, ViralDefective VirusesGenes, p53HEK293 CellsHumansInhibitor of Apoptosis ProteinsMidkineAdenovirus E1A ProteinsBIRC5 protein, humanCapsid ProteinsCASP3 protein, humanCaspase 3CDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21hexon capsid protein, AdenovirusInhibitor of Apoptosis ProteinsMDK protein, humanMDM2 protein, humanMidkineNerve Growth FactorsPoly(ADP-ribose) PolymerasesProto-Oncogene Proteins c-mdm2SurvivinTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID26251031
OpenAlexW1055886613

What OpenQuestion holds

Textmetadata
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.