Evidence map›Paper›PMID 29535833›Full record

ArticleOncotarget2018

Glucagon promotes colon cancer cell growth via regulating AMPK and MAPK pathways.

Takashi Yagi, Eiji Kubota, Hiroyuki Koyama, Tomohiro Tanaka, Hiromi Kataoka, Kenro Imaeda, Takashi Joh

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

20 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
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  6. Article
  7. Glucagon Enhances Chemotherapy Efficacy By Inhibition of Tumor Vessels in Colorectal Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Constructing a thyroid cancer prognostic risk model based on CD8Central-European journal of immunology · 2022
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

7 authors at 1 institution in 1 country.

Takashi YagiDepartment of Gastroenterology and Metabolism, Nagoya City University Graduate School of Medical Sciences, Mizuho-ku, Nagoya 467-8601, Japan.
Eiji KubotaDepartment of Gastroenterology and Metabolism, Nagoya City University Graduate School of Medical Sciences, Mizuho-ku, Nagoya 467-8601, Japan.
Hiroyuki KoyamaDepartment of Gastroenterology and Metabolism, Nagoya City University Graduate School of Medical Sciences, Mizuho-ku, Nagoya 467-8601, Japan.
Tomohiro TanakaDepartment of Gastroenterology and Metabolism, Nagoya City University Graduate School of Medical Sciences, Mizuho-ku, Nagoya 467-8601, Japan.
Hiromi KataokaDepartment of Gastroenterology and Metabolism, Nagoya City University Graduate School of Medical Sciences, Mizuho-ku, Nagoya 467-8601, Japan.
Kenro ImaedaDepartment of Gastroenterology and Metabolism, Nagoya City University Graduate School of Medical Sciences, Mizuho-ku, Nagoya 467-8601, Japan.
Takashi JohDepartment of Gastroenterology and Metabolism, Nagoya City University Graduate School of Medical Sciences, Mizuho-ku, Nagoya 467-8601, Japan.
Nagoya City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer is one of the major causes of death in diabetic patients, and an association between antidiabetic drugs and cancer risk has been reported. Such evidence implies a strong connection between diabetes and cancer. Recently, glucagon has been recognized as a pivotal factor implicated in the pathophysiology of diabetes. Glucagon acts through binding to its receptor, glucagon receptor (GCGR), and cross-talk between GCGR-mediated signals and signaling pathways that regulate cancer cell fate has been unveiled. In the current study, expression of GCGR in colon cancer cell lines and colon cancer tissue obtained from patients was demonstrated. Glucagon significantly promoted colon cancer cell growth, and GCGR knockdown with small interfering RNA attenuated the proliferation-promoting effect of glucagon on colon cancer cells. Molecular assays showed that glucagon acted as an activator of cancer cell growth through deactivation of AMPK and activation of MAPK in a GCGR-dependent manner. Moreover, a stable GCGR knockdown mouse colon cancer cell line, CMT93, grew significantly slower than control in a syngeneic mouse model of type 2 diabetes with glycemia and hyperglucagonemia. The present observations provide experimental evidence that hyperglucagonemia in type 2 diabetes promotes colon cancer progression via GCGR-mediated regulation of AMPK and MAPK pathways.

Indexed as

colon cancerglucagonglucagon signallingincretinproliferation

Identifiers

PMID29535833
PMCPMC5828215
OpenAlexW2792821257

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.