Evidence map›Paper›PMID 35517411›Full record

ArticleJournal of Cancer2022

PlexinA1 activation induced by β2-AR promotes epithelial-mesenchymal transition through JAK-STAT3 signaling in human gastric cancer cells.

Ying Liu, Yanhui Hao, Hanzheng Zhao, Ying Zhang, Die Cheng, Li Zhao, Yuqiao Peng, Yanjie Lu, Yuhong Li

Open access · goldAbstract read
In one paragraph

Article in Journal of Cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 14 citations in OpenAlex.

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    Observational
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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

9 authors at 3 institutions in 1 country.

Ying LiuDepartment of Pathology, Chengde Medical University, Chengde, Hebei, China.
Yanhui HaoBeijing Institute of Radiation Medicine, Beijing, China.
Hanzheng ZhaoDepartment of General Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Ying ZhangDepartment of clinical laboratory, The First Affiliated Hospital of Chengde Medical College, Chengde, Hebei, China.
Die ChengDepartment of Pathology, Chengde Medical University, Chengde, Hebei, China.
Li ZhaoDepartment of Ultrasound Medicine, The First Affiliated Hospital of Chengde Medical College, Chengde, Hebei, China.
Yuqiao PengDepartment of Pathology, Chengde Medical University, Chengde, Hebei, China.
Yanjie LuDepartment of Pathology, Chengde Medical University, Chengde, Hebei, China.
Yuhong LiDepartment of Pathology, Chengde Medical University, Chengde, Hebei, China.
Chengde Medical University · CNBeijing Radiation Center · CNHarbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

With the medical model shifting from a single biomedical model to a biopsychological-social model, the impact of psychosocial factors on cancer patients has attracted attention. Studies have shown that chronic stress caused by long-term psychological stress, such as anxiety and depression, can promote the malignant progression of tumors by acting on β2-adrenergic receptor (β2-AR). β2-AR can promote tumor migration by activating epithelial-mesenchymal transition (EMT). However, the underlying mechanisms in the regulation of EMT by β2-AR are still unclear. In this study, we established a chronic stress model by treating MGC-803 and SGC-7901 human gastric cancer cells with isoproterenol (ISO), a β2-AR agonist. EMT in the two gastric cancer cell lines was enhanced after ISO treatment. Thereafter, we found that the interaction between β2-AR and PlexinA1 was involved in the process by which chronic stress affects EMT in both MGC-803 and SGC-7901 cells. Moreover, the activation of β2-AR by ISO increased the expression of PlexinA1, activated JAK-STAT3 signaling and further promoted EMT in human gastric cancer cells. Importantly, the knockdown of PlexinA1 by small hairpin RNAs inhibited JAK-STAT3 signaling and abolished the EMT induced by β2-AR. In conclusion, PlexinA1 was an important downstream target of β2-AR, through which β2-AR promoted EMT in human gastric cancer cells by activating JAK-STAT3 signaling.

Indexed as

chronic stressepithelial-mesenchymal transitiongastric cancerJAK-STAT3PlexinA1β2-AR

Identifiers

PMID35517411
PMCPMC9066200
OpenAlexW4285168154

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.