Evidence map›Paper›PMID 31782107›Full record

ArticleHuman cell2020

Tumor promoting effects of glucagon receptor: a promising biomarker of papillary thyroid carcinoma via regulating EMT and P38/ERK pathways.

Hong-Chun Jiang, Xiang-Ru Chen, Hai-Feng Sun, Yuan-Wen Nie

Abstract read
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In one paragraph

Article in Human cell, 2020. 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
3.0field-weighted citation impact, top 8% 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, 11 citations in OpenAlex.

  1. Article
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  5. Constructing a thyroid cancer prognostic risk model based on CD8Central-European journal of immunology · 2022
    Article
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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

4 authors at 1 institution in 1 country.

Hong-Chun JiangEye 3 Division of Red Flag Hospital of Mudanjiang Medical University, Mudanjiang, 157000, Heilongjiang, People's Republic of China.
Xiang-Ru ChenColor Doppler Ultrasound Room, The Second Affiliated Hospital of Mudanjiang Medical University, Mudanjiang, 157000, Heilongjiang, People's Republic of China.
Hai-Feng SunDepartment of Endocrinology, The Second Affiliated Hospital of Mudanjiang Medical University, Mudanjiang, 157000, Heilongjiang, People's Republic of China.
Yuan-Wen NieHepatobiliary Surgery, The Second Affiliated Hospital of Mudanjiang Medical University, Mudanjiang, 157000, Heilongjiang, People's Republic of China. mdjnyw@163.com.ORCID http://orcid.org/0000-0003-4390-4272
Mudanjiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucagon is a crucial hormone involved in the maintenance of glucose homeostasis. Large efforts to define the role of glucagon receptor (GCGR) have been continuously made in recent years, but it is still incomplete about its function and mechanism. We performed this study to verify its potential impacts on papillary thyroid carcinoma (PTC) progression. Correlation between GCGR expression and PTC was elaborated using The Cancer Genome Atlas (TCGA) database. The Kaplan-Meier method was used to analyze the connection between GCGR expression and prognosis of PTC patients. GCGR expression was measured by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot analysis; simultaneously, cell viability was elucidated using cell proliferation and colony formation assays following siRNAs strategy. Transwell analyses were conducted to measure the invasion and migration of PTC cells. Flow cytometry analysis was conducted to examine apoptotic ability. The cAMP ELISA kit was employed to measure the cAMP level in PTC cells. Our data determined that the expression level of GCGR was increased in PTC tissues and cells in contrast to normal tissues and Nthy-ori 3-1, respectively. Up-regulated GCGR expression was linked with the lower survival rate in patients with PTC. Functional analysis in vitro suggested that GCGR knockdown attenuated PTC cell proliferation, colony formation, invasion, and migration whilst intensified apoptosis. Down-regulated GCGR was able to increase cAMP level. Furthermore, reduction of GCGR could result in the inactivation of epithelial-mesenchymal transition (EMT) and P38/ERK pathways. In conclusion, the findings of this study disclosed that GCGR promoted PTC cell behaviors by mediating the EMT and P38/ERK pathways, serving as a potential diagnostic and prognostic biomarker as well as therapeutic target for PTC.

Indexed as

Receptors, GlucagonBiomarkers, TumorHumansMAP Kinase Signaling SystemOrganic Cation Transporter 3Organic Cation Transport ProteinsThyroid Cancer, PapillaryThyroid NeoplasmsBiomarkers, TumorOrganic Cation Transporter 3Organic Cation Transport ProteinsReceptors, GlucagonCell vitalityEMTGCGRP38/ERKPapillary thyroid carcinoma

Identifiers

PMID31782107
OpenAlexW2990771620

What OpenQuestion holds

Textmetadata
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.