Evidence map›Paper›PMID 23603476›Full record

ArticleToxicology in vitro : an international journal published in association with BIBRA2013

Activation of ERK signaling and induction of colon cancer cell death by piperlongumine.

H Randhawa, K Kibble, H Zeng, M P Moyer, K M Reindl

Abstract read
In one paragraph

Article in Toxicology in vitro : an international journal published in association with BIBRA, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
13.5field-weighted citation impact, top 1% 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

54 citing papers in PubMed, 95 citations in OpenAlex.

  1. Migrasomes: A Novel Target for Cancer Treatment.Current cancer drug targets · 2026
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  3. Phytochemicals FromJournal of skin cancer · 2025
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  7. The Antitumor Activity of Piplartine: A Review.Pharmaceuticals (Basel, Switzerland) · 2023
    Review
  8. Article
  9. Article
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  11. Frontiers in pharmacology · 2023
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Chitosan degradation products promote healing of burn wounds of rat skin.Frontiers in bioengineering and biotechnology · 2022
    Article
  17. Review
  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

5 authors at 3 institutions in 1 country.

H RandhawaDepartment of Biological Sciences, North Dakota State University, Fargo, ND 51808-6050, USA.
K Kibble
H Zeng
M P Moyer
K M Reindl
North Dakota State University · USGrand Forks Human Nutrition Research Center · USIncell Corporation (United States) · US

Funding

TARGETING AND DELIVERYP20RR015566 · NCRR · NORTH DAKOTA STATE UNIVERSITY · PI DORSAM, GLENN PAUL · 2001 to 2011
$19.0M
Pilot Projects: Core DP30GM103332 · NIGMS · NORTH DAKOTA STATE UNIVERSITY · PI SIBI, MUKUND P. · 2012 to 2016
$4.9M
NCRR NIH HHS 2P20 RR015566NCRR NIH HHS P20 RR015566NIGMS NIH HHS P30 GM103332
6 · The paper itself

Abstract

Piperlongumine (PPLGM) is a bioactive compound isolated from long peppers that shows selective toxicity towards a variety of cancer cell types including colon cancer. The signaling pathways that lead to cancer cell death in response to PPLGM exposure have not been previously identified. Our objective was to identify the intracellular signaling mechanisms by which PPLGM leads to enhanced colon cancer cell death. We found that PPLGM inhibited the growth of colon cancer cells in time- and concentration-dependent manners, but was not toxic toward normal colon mucosal cells at concentrations below 10 μM. Acute (0-60 min) and prolonged (24h) exposure of HT-29 cells to PPLGM resulted in phosphorylation of ERK. To investigate whether ERK signaling was involved in PPLGM-mediated cell death, we treated HT-29 cells with the MEK inhibitor U0126, prior to treating with PPLGM. We found that U0126 attenuated PPLGM-induced activation of ERK and partially protected against PPLGM-induced cell death. These results suggest that PPLGM works, at least in part, through the MEK/ERK pathway to result in colon cancer cell death. A more thorough understanding of the molecular mechanisms by which PPLGM induces colon cancer cell death will be useful in developing therapeutic strategies to treat colon cancer.

Indexed as

Antineoplastic AgentsApoptosisCell LineColonColonic NeoplasmsDioxolanesExtracellular Signal-Regulated MAP KinasesHCT116 CellsHT29 CellsHumansIntestinal MucosaMAP Kinase Signaling SystemPiperidonesSignal TransductionAntineoplastic AgentsDioxolanesExtracellular Signal-Regulated MAP KinasesPiperidonespiperlongumineApoptosisCell signalingColon cancerERKextracellular-signal-regulated kinaseMAPKMEKMEK/ERKmitogen-activated protein kinasepiperlonguminePiperlonguminePPLGMRASrat sarcoma oncogenereactive oxygen speciesROS

Identifiers

PMID23603476
PMCPMC3749270
OpenAlexW2039093333

What OpenQuestion holds

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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.