Evidence map›Paper›PMID 23941827›Full record

ArticleCancer letters2013

Carboxypeptidase E promotes cancer cell survival, but inhibits migration and invasion.

Saravana R K Murthy, Evan Dupart, Najla Al-Sweel, Alexander Chen, Niamh X Cawley, Y Peng Loh

Open access · greenAbstract read
In one paragraph

Article in Cancer letters, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

27 citing papers in PubMed, 37 citations in OpenAlex.

  1. Physical exercise increases binding of POMC to blood extracellular vesicles.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

6 authors at 1 institution in 1 country.

Saravana R K Murthy *Section on Cellular Neurobiology, Program on Developmental Biology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD 20892. USA.
Evan Dupart *Section on Cellular Neurobiology, Program on Developmental Biology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD 20892. USA.
Najla Al-SweelSection on Cellular Neurobiology, Program on Developmental Biology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD 20892. USA.
Alexander ChenSection on Cellular Neurobiology, Program on Developmental Biology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD 20892. USA.
Niamh X CawleySection on Cellular Neurobiology, Program on Developmental Biology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD 20892. USA.
Y Peng LohSection on Cellular Neurobiology, Program on Developmental Biology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD 20892. USA.
Eunice Kennedy Shriver National Institute of Child Health and Human Development · US

Funding

The Role of Carboxypeptidase E in CancerZIAHD008804 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI LOH, YOKE PENG · 2009 to 2019
$6.1M
Intramural NIH HHS Z99 DA999999Intramural NIH HHS Z99 HD999999Intramural NIH HHS Z99 HL999999Intramural NIH HHS Z99 MH999999Intramural NIH HHS Z99 OD999999Intramural NIH HHS ZIA HD008804
6 · The paper itself

Abstract

Carboxypeptidase E (CPE), a prohormone processing enzyme is highly expressed and secreted from (neuro)endocrine tumors and gliomas, and has been implicated in cancer progression by promoting tumor growth. Our study demonstrates that secreted or exogenously applied CPE promotes survival of pheochromocytoma (PC12) and hepatocellular carcinoma (MHCC97H) cells under nutrient starvation and hypoxic conditions, but had no effect on their proliferation. CPE also reduced migration and invasion of fibrosarcoma (HT1080) cells. We show that CPE treatment mediates survival of MHCC97H cells during metabolic stress by up-regulating the expression of anti-apoptotic protein BCL-2, and other pro-survival genes, via activation of the ERK1/2 pathway.

Indexed as

Cell ProliferationAnimalsAntibodies, MonoclonalCarboxypeptidase HCell Line, TumorCell MovementCell SurvivalGene Expression Regulation, NeoplasticHumansImmunoblottingMAP Kinase Signaling SystemMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Neoplasm InvasivenessNeoplasmsPC12 CellsAntibodies, MonoclonalCarboxypeptidase HMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Proto-Oncogene Proteins c-bcl-2Recombinant ProteinsCell invasionCell survivalFibrosarcomaHepatocellular carcinomaPheochromocytoma

Identifiers

PMID23941827
PMCPMC3825807
OpenAlexW2021732474

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.