Evidence map›Paper›PMID 26876199›Full record

ArticleOncogene2016

Disruption of insulin receptor function inhibits proliferation in endocrine-resistant breast cancer cells.

J Y Chan, K LaPara, D Yee

Abstract 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 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.5field-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

26 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. IGF-1 Stimulates Glycolytic ATP Production in MCF-7L Cells.International journal of molecular sciences · 2023
    Article
  5. Review
  6. ACBD3 Bioinformatic Analysis and Protein Expression in Breast Cancer Cells.International journal of molecular sciences · 2022
    Article
  7. Article
  8. Obesity and endocrine therapy resistance in breast cancer: Mechanistic insights and perspectives.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2022
    Review
  9. Review
  10. DDAB cationic lipid-mPEG, PCL copolymer hybrid nano-carrier synthesis and application for delivery of siRNA targeting IGF-1R into breast cancer cells.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021
    Article
  11. Disrupting Insulin and IGF Receptor Function in Cancer.International journal of molecular sciences · 2021
    Review
  12. Article
  13. Article
  14. Obesity, Type 2 Diabetes, and Cancer Risk.Frontiers in oncology · 2020
    Review
  15. Article
  16. Review
  17. Article
  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

3 authors at 2 institutions in 1 country.

J Y ChanDepartment of Pharmacology, University of Minnesota, Minneapolis, MN, USA.
K LaParaMasonic Cancer Center, University of Minnesota, Minneapolis, MN, USA.
D YeeDepartment of Pharmacology, University of Minnesota, Minneapolis, MN, USA.
University of Minnesota Medical Center · USUniversity of Minnesota · US

Funding

Women's CancerP30CA077598 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI Douglas Yee · 1998 to 2026
$100.4M
The Role of CHFR in Tumorigenesis and Paclitaxel-Sensitivity in Breast CancerP50CA116201 · NCI · MAYO CLINIC ROCHESTER · PI PETER C LUCAS · 2005 to 2026
$49.9M
NCI NIH HHS P30 CA077598NCI NIH HHS P50 CA116201
6 · The paper itself

Abstract

The insulin-like growth factor (IGF) system is a well-studied growth regulatory pathway implicated in breast cancer biology. Clinical trials testing monoclonal antibodies directed against the type I IGF receptor (IGF1R) in combination with estrogen receptor-α (ER) targeting have been completed, but failed to show benefits in patients with endocrine-resistant tumors compared to ER targeting alone. We have previously shown that the closely related insulin receptor (InsR) is expressed in tamoxifen-resistant (TamR) breast cancer cells. Here we examined if inhibition of InsR affected TamR breast cancer cells. InsR function was inhibited by three different mechanisms: InsR short hairpin RNA, a small InsR-blocking peptide, S961 and an InsR monoclonal antibody (mAb). Suppression of InsR function by these methods in TamR cells successfully blocked insulin-mediated signaling, monolayer proliferation, cell cycle progression and anchorage-independent growth. This strategy was not effective in parental cells likely because of the presence of IGFR /InsR hybrid receptors. Downregulation of IGF1R in conjunction with InsR inhibition was more effective in blocking IGF- and insulin-mediated signaling and growth in parental cells compared with single-receptor targeting alone. Our findings show TamR cells were stimulated by InsR and were not sensitive to IGF1R inhibition, whereas in tamoxifen-sensitive parental cancer cells, the presence of both receptors, especially hybrid receptors, allowed cross-reactivity of ligand-mediated activation and growth. To suppress the IGF system, targeting of both IGF1R and InsR is optimal in endocrine-sensitive and -resistant breast cancer.

Indexed as

Antibodies, MonoclonalBreast NeoplasmsCell ProliferationDrug Resistance, NeoplasmGene Knockdown TechniquesHumansMAP Kinase Signaling SystemMCF-7 CellsPeptidesPhosphatidylinositol 3-KinasesReceptor, IGF Type 1Receptor, InsulinReceptors, SomatomedinRNA, Small InterferingSignal TransductionTamoxifenAntibodies, MonoclonalIGF1R protein, humanPeptidesPhosphatidylinositol 3-KinasesReceptor, IGF Type 1Receptor, InsulinReceptors, SomatomedinRNA, Small InterferingS961 peptideTamoxifen

Identifiers

PMID26876199
PMCPMC4982805
OpenAlexW2281022131

What OpenQuestion holds

Textmetadata
LicenceTDM
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.