Evidence map›Paper›PMID 35561088›Full record

ArticleCancer science2022

IFN-α/β-mediated NK2R expression is related to the malignancy of colon cancer cells.

Huihui Xiang, Yujiro Toyoshima, Weidong Shen, Xiangdong Wang, Naoki Okada, Shuhei Kii, Ko Sugiyama, Toshihiro Nagato, Hiroya Kobayashi, Kazuho Ikeo and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2022. 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
1.6field-weighted citation impact, top 18% 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, 18 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 4 institutions in 2 countries.

Huihui XiangDivision of Functional Immunology, Section of Disease Control, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan.
Yujiro ToyoshimaDivision of Functional Immunology, Section of Disease Control, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan.
Weidong ShenDivision of Functional Immunology, Section of Disease Control, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan.
Xiangdong WangDivision of Functional Immunology, Section of Disease Control, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan.
Naoki OkadaDivision of Functional Immunology, Section of Disease Control, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan.
Shuhei KiiDivision of Functional Immunology, Section of Disease Control, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan.
Ko SugiyamaDivision of Functional Immunology, Section of Disease Control, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan.
Toshihiro NagatoDepartment of Pathology, Asahikawa Medical University, Asahikawa, Japan.
Hiroya KobayashiDepartment of Pathology, Asahikawa Medical University, Asahikawa, Japan.
Kazuho IkeoDNA Data Analysis Laboratory, National Institute of Genetics, Mishima, Japan.
Shinichi HashimotoDepartment of Molecular Pathophysiology, Institute of Advanced Medicine, Wakayama Medical University, Wakayama, Japan.
Mishie TaninoDepartment of Surgical Pathology, Asahikawa Medical University, Asahikawa, Japan.
Akinobu TaketomiDepartment of Gastroenterological Surgery I, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Hidemitsu KitamuraDivision of Functional Immunology, Section of Disease Control, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan.ORCID https://orcid.org/0000-0001-7006-6767
Hokkaido University · JPAsahikawa Medical University · JPNational Institute of Genetics · JPWakayama Medical University · JP

Funding

Japan Society for the Promotion of Science 15K08416Japan Society for the Promotion of Science 16H05409Japan Society for the Promotion of Science 25460584
6 · The paper itself

Abstract

Neurokinin 2 receptor (NK2R), a G protein-coupled receptor for neurokinin A (NKA), a tachykinin family member, regulates various physiological functions including pain response, relaxation of smooth muscle, dilation of blood vessels, and vascular permeability. However, the precise role and regulation of NK2R expression in cancer cells have not been fully elucidated. In this study, we found that high NK2R gene expression was correlated with the poor survival of colorectal cancer patients, and Interferon (IFN-α/β) stimulation significantly enhanced NK2R gene expression level of colon cancer cells in a Janus kinas 1/2 (JAK 1/2)-dependent manner. NKA stimulation augmented viability/proliferation and phosphorylation of Extracellular-signal-regulated kinase 1/2 (ERK1/2) levels of IFN-α/β-treated colon cancer cells and NK2R blockade by using a selective antagonist reduced the proliferation in vitro. Administration of an NK2R antagonist alone or combined with polyinosinic-polycytidylic acid, a synthetic analog of double-stranded RNA, to CT26-bearing mice significantly suppressed tumorigenesis. NK2R-overexpressing CT26 cells showed enhanced tumorigenesis and metastatic colonization in both lung and liver after the inoculation into mice. These findings indicate that IFN-α/β-mediated NK2R expression is related to the malignancy of colon cancer cells, suggesting that NK2R blockade may be a promising strategy for colon cancers.

Indexed as

Colonic NeoplasmsInterferon-betaNeurokinin AReceptors, Neurokinin-2AnimalsCarcinogenesisGene ExpressionHumansInterferon-alphaMiceInterferon-alphaInterferon-betaNeurokinin AReceptors, Neurokinin-2colon cancerJAKmalignancyneurokinin-2 receptortype I IFN

Identifiers

PMID35561088
PMCPMC9357608
OpenAlexW4280512768

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.