Evidence map›Paper›PMID 30607005›Full record

ArticleCancer gene therapy2019

Overexpression of SOCS3 mediated by adenovirus vector in mouse and human castration-resistant prostate cancer cells increases the sensitivity to NK cells in vitro and in vivo.

Tomomi Yoneda, Naoto Kunimura, Koichi Kitagawa, Yuka Fukui, Hiroki Saito, Keita Narikiyo, Motoki Ishiko, Naoki Otsuki, Ken-Ichi Nibu, Masato Fujisawa and 3 more

Abstract read
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In one paragraph

Article in Cancer gene therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 5 pooled it
1.6field-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

21 citing papers in PubMed, 5 syntheses or guidelines pooled it, 23 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 2 institutions in 1 country.

Tomomi YonedaDivision of Advanced Medical Science, Kobe University Graduate School of Science, Technology and Innovation, Kobe, Japan.
Naoto KunimuraDivision of Advanced Medical Science, Kobe University Graduate School of Science, Technology and Innovation, Kobe, Japan.
Koichi KitagawaDivision of Advanced Medical Science, Kobe University Graduate School of Science, Technology and Innovation, Kobe, Japan.
Yuka FukuiDivision of Advanced Medical Science, Kobe University Graduate School of Science, Technology and Innovation, Kobe, Japan.
Hiroki SaitoDivision of Advanced Medical Science, Kobe University Graduate School of Science, Technology and Innovation, Kobe, Japan.
Keita NarikiyoDivision of Advanced Medical Science, Kobe University Graduate School of Science, Technology and Innovation, Kobe, Japan.
Motoki IshikoDivision of Advanced Medical Science, Kobe University Graduate School of Science, Technology and Innovation, Kobe, Japan.
Naoki OtsukiDivision of Otolaryngology, Kobe University Graduate School of Medicine, Kobe, Japan.ORCID http://orcid.org/0000-0002-9682-2548
Ken-Ichi NibuDivision of Otolaryngology, Kobe University Graduate School of Medicine, Kobe, Japan.
Masato FujisawaDivision of Urology, Kobe University Graduate School of Medicine, Kobe, Japan.
Satoshi SeradaCenter for Intractable Immune Disease, Kochi Medical School, Kochi University, Kochi, Japan.
Tetsuji NakaCenter for Intractable Immune Disease, Kochi Medical School, Kochi University, Kochi, Japan.
Toshiro ShirakawaDivision of Advanced Medical Science, Kobe University Graduate School of Science, Technology and Innovation, Kobe, Japan. toshiro@med.kobe-u.ac.jp.
Kobe University · JPKōchi University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer is one of the most common cancers in men. The overactivation of IL-6/JAK/STAT3 signaling and silencing of SOCS3 are frequently observed in prostate cancer. In the present study we undertook to develop Ad-SOCS3 gene therapy for the treatment of prostate cancer and also investigated whether Ad-SOCS3 increased sensitivity to NK cells. We demonstrated that Ad-SOCS3 could significantly inhibit growth of castration-resistant prostate cancer (CRPC) cell lines expressing pSTAT3, DU-145 (at 10, 20, and 40 MOI), and TRAMP-C2 (at 40 MOI), but not the PC-3 CRPC cell line with the STAT3 gene deleted. Ad-SOCS3 (40 MOI) could suppress IL-6 production in DU-145 cells and PD-L1 expression induced by IFN-γ in TRAMP-C2 cells, and increased the NK cell sensitivity of both TRAMP-C2 and DU-145 cells. In the DU-145 mouse xenograft tumor model, intratumoral injections (twice/week for 3 weeks) of 1 × 10

Indexed as

Gene ExpressionAdenoviridaeAnimalsApoptosisBiomarkers, TumorCell CycleCell Line, TumorDisease Models, AnimalGenetic VectorsGene Transfer TechniquesHumansInterleukin-6Killer Cells, NaturalMaleMiceProstatic Neoplasms, Castration-ResistantBiomarkers, TumorInterleukin-6SOCS3 protein, humanSuppressor of Cytokine Signaling 3 Protein

Identifiers

PMID30607005
OpenAlexW2908014170

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.