Evidence map›Paper›PMID 35504863›Full record

ArticleOncogenesis2022

Cytoglobin attenuates pancreatic cancer growth via scavenging reactive oxygen species.

Dinh Viet Hoang, Le Thi Thanh Thuy, Hoang Hai, Vu Ngoc Hieu, Kenjiro Kimura, Daisuke Oikawa, Yoshihiro Ikura, Ninh Quoc Dat, Truong Huu Hoang, Misako Sato-Matsubara and 8 more

Open access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
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  8. Article
  9. Insights into the function of cytoglobin.Biochemical Society transactions · 2023
    Review
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 6 institutions in 2 countries.

Dinh Viet Hoang *Department of Hepatology, Graduate School of Medicine, Osaka Metropolitan University, Osaka, Japan.ORCID http://orcid.org/0000-0001-7844-3192
Le Thi Thanh Thuy *Department of Hepatology, Graduate School of Medicine, Osaka Metropolitan University, Osaka, Japan.ORCID http://orcid.org/0000-0003-4460-735X
Hoang HaiDepartment of Hepatology, Graduate School of Medicine, Osaka Metropolitan University, Osaka, Japan.
Vu Ngoc HieuDepartment of Hepatology, Graduate School of Medicine, Osaka Metropolitan University, Osaka, Japan.
Kenjiro KimuraDepartment of Hepato-Biliary-Pancreatic Surgery, Graduate School of Medicine, Osaka Metropolitan University, Osaka, Japan.
Daisuke OikawaDepartment of Pathobiochemistry, Graduate School of Medicine, Osaka Metropolitan University, Osaka, Japan.
Yoshihiro IkuraDepartment of Pathology, Takatsuki General Hospital, Takatsuki, Japan.ORCID http://orcid.org/0000-0001-8599-2245
Ninh Quoc DatDepartment of Pediatrics, Hanoi Medical University, Hanoi, Vietnam.
Truong Huu HoangDepartment of Hepatology, Graduate School of Medicine, Osaka Metropolitan University, Osaka, Japan.
Misako Sato-MatsubaraDepartment of Hepatology, Graduate School of Medicine, Osaka Metropolitan University, Osaka, Japan.
Minh Phuong DongDepartment of Hepatology, Graduate School of Medicine, Osaka Metropolitan University, Osaka, Japan.
Ngo Vinh HanhDepartment of Hepatology, Graduate School of Medicine, Osaka Metropolitan University, Osaka, Japan.
Sawako Uchida-KobayashiDepartment of Hepatology, Graduate School of Medicine, Osaka Metropolitan University, Osaka, Japan.
Fuminori TokunagaDepartment of Pathobiochemistry, Graduate School of Medicine, Osaka Metropolitan University, Osaka, Japan.
Shoji KuboDepartment of Hepato-Biliary-Pancreatic Surgery, Graduate School of Medicine, Osaka Metropolitan University, Osaka, Japan.
Naoko OhtaniDepartment of Pathophysiology, Graduate School of Medicine, Osaka Metropolitan University, Osaka, Japan.
Katsutoshi YoshizatoDonated Laboratory for Synthetic Biology, Graduate School of Medicine, Osaka Metropolitan University, Osaka, Japan.
Norifumi KawadaDepartment of Hepatology, Graduate School of Medicine, Osaka Metropolitan University, Osaka, Japan. kawadanori@omu.ac.jp.ORCID http://orcid.org/0000-0002-6392-8311
Osaka Metropolitan University · JP108 Military Central Hospital · VNCho Ray Hospital · VNHanoi Medical University · VNOsaka University of Economics · JPTakatsuki General Hospital · JP

Funding

Gilead Sciences (Gilead) FY2019-2021Japan Agency for Medical Research and Development (AMED) 21gm1010009h0004Japan Agency for Medical Research and Development (AMED) AMED- JP21fk0210050MEXT | Japan Society for the Promotion of Science (JSPS) 19H03641MEXT | Japan Society for the Promotion of Science (JSPS) 19K08428
6 · The paper itself

Abstract

Pancreatic cancer is a highly challenging malignancy with extremely poor prognosis. Cytoglobin (CYGB), a hemeprotein involved in liver fibrosis and cancer development, is expressed in pericytes of all organs. Here, we examined the role of CYGB in the development of pancreatic cancer. CYGB expression appeared predominately in the area surrounding adenocarcinoma and negatively correlated with tumor size in patients with pancreatic cancer. Directly injecting 7, 12-dimethylbenz[a]anthracene into the pancreatic tail in wild-type mice resulted in time-dependent induction of severe pancreatitis, fibrosis, and oxidative damage, which was rescued by Cygb overexpression in transgenic mice. Pancreatic cancer incidence was 93% in wild-type mice but only 55% in transgenic mice. Enhanced CYGB expression in human pancreatic stellate cells in vitro reduced cellular collagen synthesis, inhibited cell activation, increased expression of antioxidant-related genes, and increased CYGB secretion into the medium. Cygb-overexpressing or recombinant human CYGB (rhCYGB) -treated MIA PaCa-2 cancer cells exhibited dose-dependent cell cycle arrest at the G1 phase, diminished cell migration, and reduction in colony formation. RNA sequencing in rhCYGB-treated MIA PaCa-2 cells revealed downregulation of cell cycle and oxidative phosphorylation pathways. An increase in MIA PaCa-2 cell proliferation and reactive oxygen species production by H

Identifiers

PMID35504863
PMCPMC9065067
OpenAlexW4225423337

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.