Evidence map›Paper›PMID 26876198›Full record

ArticleOncogene2016

CDCP1 cleavage is necessary for homodimerization-induced migration of triple-negative breast cancer.

H J Wright, J Arulmoli, M Motazedi, L J Nelson, F S Heinemann, L A Flanagan, O V Razorenova

Open access · bronzeAbstract 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 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

31 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. ACSL3 regulates breast cancer progressionCancer biology & medicine · 2024
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. CUB Domain-Containing Protein 1 (CDCP1) Is a Target for Radioligand Therapy in Castration-Resistant Prostate Cancer, including PSMA Null Disease.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Loss of CDCP1 triggers FAK activation in detached prostate cancer cells.American journal of clinical and experimental urology · 2021
    Article
  16. Article
  17. Theranostic Targeting of CUB Domain Containing Protein 1 (CDCP1) in Pancreatic Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020
    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

7 authors at 2 institutions in 1 country.

H J WrightDepartment of Molecular Biology and Biochemistry, University of California, Irvine, CA, USA.
J ArulmoliDepartment of Biomedical Engineering, University of California, Irvine, CA, USA.
M MotazediDepartment of Molecular Biology and Biochemistry, University of California, Irvine, CA, USA.
L J NelsonDepartment of Molecular Biology and Biochemistry, University of California, Irvine, CA, USA.
F S HeinemannDepartment of Pathology, Hoag Memorial Hospital Presbyterian, Newport Beach, CA, USA.
L A FlanaganDepartment of Biomedical Engineering, University of California, Irvine, CA, USA.
O V RazorenovaDepartment of Molecular Biology and Biochemistry, University of California, Irvine, CA, USA.
University of California, Irvine · USHoag Memorial Hospital Presbyterian · US

Funding

University of California Health Participation in the National COVID Cohort Collaborative (N3C)UL1TR001414 · NCATS · UNIVERSITY OF CALIFORNIA-IRVINE · PI COOPER, DAN M, VILAIN, ERIC J. · 2015 to 2023
$35.1M
NRSA Training CoreTL1TR001415 · NCATS · UNIVERSITY OF CALIFORNIA-IRVINE · PI CAIOZZO, VINCENT JAMES, HEAD, ELIZABETH · 2015 to 2023
$4.2M
Postdoctoral Training in the Radiation ScincesT32CA121940 · NCI · STANFORD UNIVERSITY · PI GRAVES, EDWARD E. · 2007 to 2018
$2.1M
Investigating the mechanism of CDCP1 activation to block CDCP1-driven metastasisF31CA196226 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI WRIGHT, HEATHER JEANNE · 2015 to 2016
$70k
NCATS NIH HHS TL1 TR001415NCATS NIH HHS UL1 TR001414NCI NIH HHS F31 CA196226NCI NIH HHS T32 CA121940
6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) is a highly aggressive and metastatic form of breast cancer that lacks the estrogen, progesterone and HER2 receptors and is resistant to targeted and hormone therapies. TNBCs express high levels of the transmembrane glycoprotein, complement C1r/C1s, Uegf, Bmp1 (CUB)-domain containing protein 1 (CDCP1), which has been correlated with the aggressiveness and poor prognosis of multiple carcinomas. Full-length CDCP1 (flCDCP1) can be proteolytically cleaved, resulting in a cleaved membrane-bound isoform (cCDCP1). CDCP1 is phosphorylated by Src family kinases in its full-length and cleaved states, which is important for its pro-metastatic signaling. We observed that cCDCP1, compared with flCDCP1, induced a dramatic increase in phosphorylation of the migration-associated proteins: PKCδ, ERK1/2 and p38 mitogen-activated protein kinase in HEK 293T. In addition, only cCDCP1 induced migration of HEK 293T cells and rescued migration of the TNBC cell lines expressing short hairpin RNA against CDCP1. Importantly, we found that only cCDCP1 is capable of dimerization, which can be blocked by expression of the extracellular portion of cCDCP1 (ECC), indicating that dimerization occurs through CDCP1's ectodomain. We found that ECC inhibited phosphorylation of PKCδ and migration of TNBC cells in two-dimensional culture. Furthermore, ECC decreased cell invasiveness, inhibited proliferation and stimulated apoptosis of TNBC cells in three-dimensional culture, indicating that the cCDCP1 dimer is an important contributor to TNBC aggressiveness. These studies have important implications for the development of a therapeutic to block CDCP1 activity and TNBC metastasis.

Indexed as

Antigens, CDAntigens, NeoplasmApoptosisCell AdhesionCell Adhesion MoleculesCell MovementDimerizationHEK293 CellsHumansNeoplasm Proteinsp38 Mitogen-Activated Protein KinasesPhosphorylationProtein IsoformsSignal TransductionTriple Negative Breast NeoplasmsAntigens, CDAntigens, NeoplasmCDCP1 protein, humanCell Adhesion MoleculesNeoplasm Proteinsp38 Mitogen-Activated Protein KinasesProtein Isoforms

Identifiers

PMID26876198
PMCPMC4985505
OpenAlexW2285494695

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.