Evidence map›Paper›PMID 30965609›Full record

ArticleCells2019

High Glucose Concentrations Negatively Regulate the IGF1R/Src/ERK Axis through the MicroRNA-9 in Colorectal Cancer.

Ya-Chun Chen, Ming-Che Ou, Chia-Wei Fang, Tsung-Hsien Lee, Shu-Ling Tzeng

Open access · goldAbstract read
In one paragraph

Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. High glucose enhances NScientific reports · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article
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

5 authors at 4 institutions in 1 country.

Ya-Chun ChenInstitute of Medicine, Chung Shan Medical University, Taichung 402, Taiwan. big383838@hotmail.com.
Ming-Che OuDepartment of Hematology and Oncology, Tungs' Taichung MetroHarbor Hospital, Taichung 435, Taiwan. mingche.ou@gmail.com.
Chia-Wei FangDivision of Colon and Rectal Surgery, Department of Surgery, Taichung Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Taichung 427, Taiwan. forgive603@yahoo.com.tw.
Tsung-Hsien LeeInstitute of Medicine, Chung Shan Medical University, Taichung 402, Taiwan. jackth.lee@gmail.com.ORCID 0000-0001-8858-0916
Shu-Ling TzengInstitute of Medicine, Chung Shan Medical University, Taichung 402, Taiwan. cherie@csmu.edu.tw.ORCID 0000-0002-6312-4161
Chung Shan Medical University · TWChung Shan Medical University Hospital · TWTaipei Tzu Chi Hospital · TWTungs' Taichung MetroHarbor Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Studies have revealed that people with hyperglycemia have a high risk of colorectal cancer (CRC). Hyperglycemia may be responsible for supplying energy to CRC cells. However, the potential molecular mechanism for this association remains unclear. Furthermore, microRNA-9 (miR-9) has a tumor-suppressive function in CRC. Aberrant reduced expression of miR-9 is involved in the development and progression of malignancy caused by a high glucose (HG) concentration. In this study, we used an HG concentration to activate miR-9 downregulation in CRC cells. Our results indicated that miR-9 decreased the insulin-like growth factor-1 receptor (IGF1R)/Src signaling pathway and downstream cyclin B1 and N-cadherin but upregulated E-cadherin. The HG concentration not only promoted cell proliferation, increased the G1 population, and modulated epithelial-to-mesenchymal transition (EMT) protein expression and morphology but also promoted the cell migration and invasion ability of SW480 (low metastatic potential) and SW620 (high metastatic potential) cells. In addition, low glucose concentrations could reverse the effect of the HG concentration in SW480 and SW620 cells. In conclusion, our results provide new evidence for multiple signaling pathways being regulated through hyperglycemia in CRC. We propose that blood sugar control may serve as a potential strategy for the clinical management of CRC.

Indexed as

MAP Kinase Signaling SystemCadherinsCarcinoembryonic AntigenCell CycleCell Line, TumorCell MovementCell ProliferationCell ShapeColorectal NeoplasmsEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticGlucoseHumansMicroRNAsModels, BiologicalReceptor, IGF Type 1CadherinsCarcinoembryonic AntigenGlucoseMicroRNAsMIRN92 microRNA, humanReceptor, IGF Type 1src-Family Kinasescolorectal cancerepithelial to mesenchymal transitionextracellular signal-regulated kinase (ERK1/2)high concentration of glucoseinsulin-like growth factor-1 receptormetastasismicroRNA-9proliferationSrc

Identifiers

PMID30965609
PMCPMC6523516
OpenAlexW2925841500

What Socratic 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 Socratic graph.