Evidence map›Paper›PMID 23144724›Full record

ArticlePloS one2012

Englerin a selectively induces necrosis in human renal cancer cells.

Florian J Sulzmaier, Zhenwu Li, Mika L Nakashige, David M Fash, William J Chain, Joe W Ramos

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

22 citing papers in PubMed, 42 citations in OpenAlex.

  1. Mechanism of (-)-Englerin A and calcium binding on the human TRPC5 channel.Protein science : a publication of the Protein Society · 2025
    Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. NaScientific reports · 2017
    Article
  10. Article
  11. The calcium-cancer signalling nexus.Nature reviews. Cancer · 2017
    Review
  12. Englerins: A Comprehensive Review.Journal of natural products · 2017
    Review
  13. Article
  14. Synthesis of a stable and orally bioavailable englerin analogue.Bioorganic & medicinal chemistry letters · 2016
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Renal cancer-selective Englerin A induces multiple mechanisms of cell death and autophagy.Journal of experimental & clinical cancer research : CR · 2013
    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

6 authors at 2 institutions in 1 country.

Florian J SulzmaierCancer Biology Program, University of Hawaii Cancer Center, University of Hawaii at Manoa, Honolulu, Hawaii, United States of America.
Zhenwu Li
Mika L Nakashige
David M Fash
William J Chain
Joe W Ramos
University of Hawaiʻi at Mānoa · USUniversity of Hawaii Cancer Center

Funding

Cancer Research Education, Advancement, Training and Empowerment (CREATE) in the PacificR25CA244073 · NCI · UNIVERSITY OF HAWAII AT MANOA · PI Joseph Keawe'aimoku Kaholokula, LENORA WM LOO · 2020 to 2026
$1.9M
RSK-2 regulates integrin-mediated adhesion and migrationR01GM088266 · NIGMS · UNIVERSITY OF HAWAII AT MANOA · PI RAMOS, JOE WILLIAM · 2010 to 2013
$1.4M
Regulation of Cell Signaling and AdhesionR56CA093849 · NCI · UNIVERSITY OF HAWAII AT MANOA · PI RAMOS, JOE WILLIAM · 2007 to 2007
$230k
Ras activation pathways in UVR-induced epidermal transformationR03CA165128 · NCI · UNIVERSITY OF HAWAII AT MANOA · PI JI, JUNFANG, RAMOS, JOE WILLIAM · 2012 to 2013
$146k
NCI NIH HHS R03 CA165128NCI NIH HHS R25 CA244073NCI NIH HHS R56 CA093849NIGMS NIH HHS R01 GM088266NIGMS NIH HHS R01GM088266
6 · The paper itself

Abstract

The number of renal cancers has increased over the last ten years and patient survival in advanced stages remains very poor. Therefore, new therapeutic approaches for renal cancer are essential. Englerin A is a natural product with a very potent and selective cytotoxicity against renal cancer cells. This makes it a promising drug candidate that may improve current treatment standards for patients with renal cancers in all stages. However, little is known about englerin A's mode of action in targeting specifically renal cancer cells. Our study is the first to investigate the biological mechanism of englerin A action in detail. We report that englerin A is specific for renal tumor cells and does not affect normal kidney cells. We find that englerin A treatment induces necrotic cell death in renal cancer cells but not in normal kidney cells. We further show that autophagic and pyroptotic proteins are unaffected by the compound and that necrotic signaling in these cells coincided with production of reactive oxygen species and calcium influx into the cytoplasm. As the first study to analyze the biological effects of englerin A, our work provides an important basis for the evaluation and validation of the compound's use as an anti-tumor drug. It also provides a context in which to identify the specific target or targets of englerin A in renal cancer cells.

Indexed as

NecrosisAntineoplastic AgentsApoptosisAutophagyCalciumCell Line, TumorCell SurvivalChloroquineCytoplasmDose-Response Relationship, DrugHEK293 CellsHumansKidney NeoplasmsMolecular StructureReactive Oxygen SpeciesSesquiterpenes, GuaianeAntineoplastic AgentsCalciumChloroquineenglerin AReactive Oxygen SpeciesSesquiterpenes, GuaianeStaurosporine

Identifiers

PMID23144724
PMCPMC3481555
OpenAlexW1986360384

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.