Evidence map›Paper›PMID 27764776›Full record

ArticleOncotarget2016

IGF-1 contributes to the expansion of melanoma-initiating cells through an epithelial-mesenchymal transition process.

Vincent Le Coz, Chaobin Zhu, Aurore Devocelle, Aimé Vazquez, Claude Boucheix, Sandy Azzi, Cindy Gallerne, Pierre Eid, Séverine Lecourt, Julien Giron-Michel

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 13% 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, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Zeaxanthin-Rich Extract from SuperfoodMolecules (Basel, Switzerland) · 2021
    Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. 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

10 authors at 3 institutions in 1 country.

Vincent Le CozINSERM UMRS 1197, Hôpital Paul Brousse, 94807 Villejuif Cedex, France.
Chaobin ZhuINSERM UMRS 1197, Hôpital Paul Brousse, 94807 Villejuif Cedex, France.
Aurore DevocelleINSERM UMRS 1197, Hôpital Paul Brousse, 94807 Villejuif Cedex, France.
Aimé VazquezINSERM UMRS 1197, Hôpital Paul Brousse, 94807 Villejuif Cedex, France.
Claude BoucheixINSERM UMRS 1193, Hôpital Paul Brousse, 94807 Villejuif Cedex, France.
Sandy AzziINSERM UMRS 1197, Hôpital Paul Brousse, 94807 Villejuif Cedex, France.
Cindy GallerneINSERM UMRS 1197, Hôpital Paul Brousse, 94807 Villejuif Cedex, France.
Pierre EidINSERM UMRS 1197, Hôpital Paul Brousse, 94807 Villejuif Cedex, France.
Séverine LecourtINSERM UMRS 1197, Hôpital Paul Brousse, 94807 Villejuif Cedex, France.
Julien Giron-MichelINSERM UMRS 1197, Hôpital Paul Brousse, 94807 Villejuif Cedex, France.
Hôpital Paul-Brousse · FRUniversité Paris-Saclay · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Melanoma is a particularly virulent human cancer, due to its resistance to conventional treatments and high frequency of metastasis. Melanomas contain a fraction of cells, the melanoma-initiating cells (MICs), responsible for tumor propagation and relapse. Identification of the molecular pathways supporting MICs is, therefore, vital for the development of targeted treatments. One factor produced by melanoma cells and their microenvironment, insulin-like growth factor-1 (IGF- 1), is linked to epithelial-mesenchymal transition (EMT) and stemness features in several cancers.We evaluated the effect of IGF-1 on the phenotype and chemoresistance of B16-F10 cells. IGF-1 inhibition in these cells prevented malignant cell proliferation, migration and invasion, and lung colony formation in immunodeficient mice. IGF-1 downregulation also markedly inhibited EMT, with low levels of ZEB1 and mesenchymal markers (N-cadherin, CD44, CD29, CD105) associated with high levels of E-cadherin and MITF, the major regulator of melanocyte differentiation. IGF-1 inhibition greatly reduced stemness features, including the expression of key stem markers (SOX2, Oct-3/4, CD24 and CD133), and the functional characteristics of MICs (melanosphere formation, aldehyde dehydrogenase activity, side population). These features were associated with a high degree of sensitivity to mitoxantrone treatment.In this study, we deciphered new connections between IGF-1 and stemness features and identified IGF-1 as instrumental for maintaining the MIC phenotype. The IGF1/IGF1-R nexus could be targeted for the development of more efficient anti-melanoma treatments. Blocking the IGF-1 pathway would improve the immune response, decrease the metastatic potential of tumor cells and sensitize melanoma cells to conventional treatments.

Indexed as

Cell ProliferationEpithelial-Mesenchymal TransitionAnimalsAntineoplastic AgentsBiomarkers, TumorCell Line, TumorCell MovementDrug Resistance, NeoplasmFemaleInsulin-Like Growth Factor ILung NeoplasmsMelanoma, ExperimentalMice, Inbred C57BLMitoxantroneNeoplasm InvasivenessNeoplastic Stem CellsAntineoplastic AgentsBiomarkers, Tumorinsulin-like growth factor-1, mouseInsulin-Like Growth Factor IMitoxantronechemoresistanceEMTIGF-1melanoma-initiating cellsmetastasis

Identifiers

PMID27764776
PMCPMC5347710
OpenAlexW2534326027

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.