Evidence map›Paper›PMID 29371937›Full record

ArticleOncotarget2017

Molecular targeting of cell-permeable peptide inhibits pancreatic ductal adenocarcinoma cell proliferation.

Shoki Sato, Toru Nakamura, Toyomasa Katagiri, Takahiro Tsuchikawa, Toshihiro Kushibiki, Kouji Hontani, Mizuna Takahashi, Kazuho Inoko, Hironobu Takano, Hirotake Abe and 8 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 32% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Article
  3. 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

18 authors at 2 institutions in 2 countries.

Shoki SatoDepartment of Gastroenterological Surgery II, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Toru NakamuraDepartment of Gastroenterological Surgery II, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Toyomasa KatagiriDivision of Genome Medicine, Institute for Genome Research, Tokushima University, Tokushima, Japan.
Takahiro TsuchikawaDepartment of Gastroenterological Surgery II, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Toshihiro KushibikiDepartment of Gastroenterological Surgery II, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Kouji HontaniDepartment of Gastroenterological Surgery II, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Mizuna TakahashiDepartment of Gastroenterological Surgery II, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Kazuho InokoDepartment of Gastroenterological Surgery II, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Hironobu TakanoDepartment of Gastroenterological Surgery II, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Hirotake AbeDepartment of Gastroenterological Surgery II, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Shintaro TakeuchiDepartment of Gastroenterological Surgery II, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Masato OnoDepartment of Gastroenterological Surgery II, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Shota KuwabaraDepartment of Gastroenterological Surgery II, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Kazufumi UmemotoDepartment of Gastroenterological Surgery II, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Tomohiro SuzukiDepartment of Gastroenterological Surgery II, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Osamu SatoDepartment of Gastroenterological Surgery II, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Yusuke NakamuraDepartment of Medicine and Surgery, The University of Chicago, Chicago, IL, USA.
Satoshi HiranoDepartment of Gastroenterological Surgery II, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Hokkaido University · JPTokushima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background

methodTheDN-C16orf74 peptide, which corresponds to the portion of C16orf74 that interacts with CN, was synthesized, and we assessed its anti-tumor activity in proliferation assays with human PDAC cells and the underlying molecular signaling pathway. Using an orthotopic xenograft model of PDAC, we treated mice intraperitoneally with phosphate-buffered saline (PBS), control peptide, or DN-C16orf74 and analyzed the tumor-suppressive effects.

resultDN-C16orf74 inhibited the binding of C16orf74 to CN in an immunoprecipitation assay. DN-C16orf74 suppressed PDAC cell proliferation, and the level of suppression depended on the expression levels of C16orf74

conclusionThe cell-permeable peptide DN-C16orf74 has a strong anti-tumor effect against PDAC

Indexed as

C16orf74cell-permeable peptidemolecular target therapypancreatic ductal adenocarcinoma

Identifiers

PMID29371937
PMCPMC5768354
OpenAlexW2766982550

What OpenQuestion holds

Textmetadata
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.