Evidence map›Paper›PMID 18058799›Full record

ArticleMolecular carcinogenesis2008

Multiple mechanisms are involved in 6-gingerol-induced cell growth arrest and apoptosis in human colorectal cancer cells.

Seong-Ho Lee, Maria Cekanova, Seung Joon Baek

Abstract read
In one paragraph

Article in Molecular carcinogenesis, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
9.2field-weighted citation impact, top 2% 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

65 citing papers in PubMed, 212 citations in OpenAlex.

  1. The effect of ginger (Zingiber officinale Roscoe) in patients with advanced cancer.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2020
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  6. Research progress of ginger in the treatment of gastrointestinal tumors.World journal of gastrointestinal oncology · 2023
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5 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Seong-Ho LeeThe Laboratory of Environmental Carcinogenesis, Department of Pathobiology, College of Veterinary Medicine, University of Tennessee, Knoxville, Tennessee 37996-4542, USA.
Maria Cekanova
Seung Joon Baek
University of Tennessee at Knoxville · US

Funding

Anti-cancer effects by the green tea catechinsR21CA109423 · NCI · UNIVERSITY OF TENNESSEE KNOXVILLE · PI BAEK, SEUNG JOON · 2005 to 2006
$337k
NCI NIH HHS R21 CA109423
6 · The paper itself

Abstract

6-Gingerol, a natural product of ginger, has been known to possess anti-tumorigenic and pro-apoptotic activities. However, the mechanisms by which it prevents cancer are not well understood in human colorectal cancer. Cyclin D1 is a proto-oncogene that is overexpressed in many cancers and plays a role in cell proliferation through activation by beta-catenin signaling. Nonsteroidal anti-inflammatory drug (NSAID)-activated gene-1 (NAG-1) is a cytokine associated with pro-apoptotic and anti-tumorigenic properties. In the present study, we examined whether 6-gingerol influences cyclin D1 and NAG-1 expression and determined the mechanisms by which 6-gingerol affects the growth of human colorectal cancer cells in vitro. 6-Gingerol treatment suppressed cell proliferation and induced apoptosis and G(1) cell cycle arrest. Subsequently, 6-gingerol suppressed cyclin D1 expression and induced NAG-1 expression. Cyclin D1 suppression was related to inhibition of beta-catenin translocation and cyclin D1 proteolysis. Furthermore, experiments using inhibitors and siRNA transfection confirm the involvement of the PKCepsilon and glycogen synthase kinase (GSK)-3beta pathways in 6-gingerol-induced NAG-1 expression. The results suggest that 6-gingerol stimulates apoptosis through upregulation of NAG-1 and G(1) cell cycle arrest through downregulation of cyclin D1. Multiple mechanisms appear to be involved in 6-gingerol action, including protein degradation as well as beta-catenin, PKCepsilon, and GSK-3beta pathways.

Indexed as

Anti-Inflammatory Agents, Non-SteroidalAntineoplastic AgentsApoptosisbeta CateninCaco-2 CellsCatecholsCell Line, TumorCell ProliferationColorectal NeoplasmsCyclin D1Dose-Response Relationship, DrugFatty AlcoholsG1 PhaseHT29 CellsHumansLuciferasesAnti-Inflammatory Agents, Non-SteroidalAntineoplastic Agentsbeta CateninCatecholsCyclin D1Fatty AlcoholsgingerolLuciferasesMAS1 protein, humanProto-Oncogene Mas

Identifiers

PMID18058799
PMCPMC2430145
OpenAlexW2029286778

What OpenQuestion holds

Textmetadata
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.