Evidence map›Paper›PMID 26096932›Full record

ArticleOncogene2016

Integrin α1β1 expression is controlled by c-MYC in colorectal cancer cells.

S Boudjadi, J C Carrier, J-F Groulx, J-F Beaulieu

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

38 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Significant position of C-myc in colorectal cancer: a promising therapeutic target.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Review
  11. Article
  12. Article
  13. Roles of Integrins in Gastrointestinal Cancer Metastasis.Frontiers in molecular biosciences · 2021
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. KFrontiers in pharmacology · 2020
    Article
  19. Novel genetic variants ofAmerican journal of cancer research · 2020
    Article
  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

4 authors at 1 institution in 1 country.

S BoudjadiLaboratory of Intestinal Physiopathology, Department of Anatomy and Cell Biology, Université de Sherbrooke, Sherbrooke, QC, Canada.
J C CarrierLaboratory of Intestinal Physiopathology, Department of Anatomy and Cell Biology, Université de Sherbrooke, Sherbrooke, QC, Canada.
J-F GroulxLaboratory of Intestinal Physiopathology, Department of Anatomy and Cell Biology, Université de Sherbrooke, Sherbrooke, QC, Canada.
J-F BeaulieuLaboratory of Intestinal Physiopathology, Department of Anatomy and Cell Biology, Université de Sherbrooke, Sherbrooke, QC, Canada.
Université de Sherbrooke · CA

Funding

Canadian Institutes of Health Research MOP-123415Canadian Institutes of Health Research MOP-97836
6 · The paper itself

Abstract

The α1β1 collagen receptor is only present in a few epithelial cell types. In the intestine, it is specifically expressed in proliferating crypt cells. This integrin has been reported to be involved in various cancers where it mediates the downstream activation of the Ras/ERK proliferative pathway. We have recently shown that integrin α1β1 is present in two-thirds of colon adenocarcinomas, but the mechanism by which ITGA1 expression is regulated is not known. DNA methylation, involved in ITGA1 repression during megakaryocyte differentiation, is not the mechanism of ITGA1 regulation in colorectal cancer cells. Our in silico analysis of the ITGA1 promoter revealed two response elements for MYC, an oncogenic factor known to regulate cancer cell proliferation, invasion and migration. In situ, the expressions of both MYC and ITGA1 are localized in the lower crypt of the normal colon and correlate in 72% of the 65 analyzed colorectal cancers. MYC pharmacological inhibition or downregulation of expression with short hairpin RNA in HT29, T84 and SW480 cells resulted in reduced ITGA1 expression at both the transcript and protein levels. Chromatin immunoprecipitation assays revealed that MYC was bound to the chromatin region of the ITGA1 proximal promoter, whereas MYC overexpression enhanced ITGA1 promoter activity that was reduced with MAD co-transfection or by the disruption of the response elements. We concluded that MYC is a key regulating factor for the control of ITGA1 expression.

Indexed as

Caco-2 CellsCell Line, TumorColorectal NeoplasmsGene Expression Regulation, NeoplasticHCT116 CellsHT29 CellsHumansIntegrin alpha1beta1Promoter Regions, GeneticProto-Oncogene Proteins c-mycIntegrin alpha1beta1Proto-Oncogene Proteins c-myc

Identifiers

PMID26096932
PMCPMC4820680
OpenAlexW818174151

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.