Evidence map›Paper›PMID 29391517›Full record

ArticleScientific reports2018

Curcumin targets multiple enzymes involved in the ROS metabolic pathway to suppress tumor cell growth.

Yonika Arum Larasati, Noriko Yoneda-Kato, Ikuko Nakamae, Takashi Yokoyama, Edy Meiyanto, Jun-Ya Kato

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04661267 (A Randomized, Double-Blind, Placebo-Controlled Trial of Regenexx Stem Cell Support Formula), which is not on this map. Cited by 99 papers.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed
8.3field-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.

NCT04661267 nacompletednot on this mapstarted 2021, after this paper: background citation

A Randomized, Double-Blind, Placebo-Controlled Trial of Regenexx Stem Cell Support Formula

TypeinterventionalSponsorRegenexx, LLCRan2021 to 2022Enrolled80ConditionsKnee OsteoarthritisArmsStem Cell Support Formula, Placebo
3 · Its place in the literature

Who cites it

99 citing papers in PubMed, 200 citations in OpenAlex.

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39 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

6 authors at 2 institutions in 2 countries.

Yonika Arum LarasatiLaboratory of Tumor Cell Biology, Graduate School of Biological Sciences, Nara Institute of Science and Technology, Ikoma, Nara, 630-0101, Japan.
Noriko Yoneda-KatoLaboratory of Tumor Cell Biology, Graduate School of Biological Sciences, Nara Institute of Science and Technology, Ikoma, Nara, 630-0101, Japan.
Ikuko NakamaeLaboratory of Tumor Cell Biology, Graduate School of Biological Sciences, Nara Institute of Science and Technology, Ikoma, Nara, 630-0101, Japan.
Takashi YokoyamaLaboratory of Tumor Cell Biology, Graduate School of Biological Sciences, Nara Institute of Science and Technology, Ikoma, Nara, 630-0101, Japan.
Edy MeiyantoCancer Chemoprevention Research Center, Faculty of Pharmacy, Universitas Gadjah Mada, Yogyakarta, Indonesia.
Jun-Ya KatoLaboratory of Tumor Cell Biology, Graduate School of Biological Sciences, Nara Institute of Science and Technology, Ikoma, Nara, 630-0101, Japan. jkata@bs.naist.jp.
Nara Institute of Science and Technology · JPUniversitas Gadjah Mada · ID

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Curcumin has been reported to exhibit anti-tumorigenic activity; however, since its precise actions remain unclear, its effects are considered to be deceptive. In the present study, we confirmed the anti-tumorigenic effects of curcumin on CML-derived leukemic cells in a xenograft model and in vitro culture system. In vitro pull-down and mass analyses revealed a series of enzymes (carbonyl reductase, glutathione-S-transferase, glyoxalase, etc.) that function in a reactive oxygen species (ROS) metabolic pathway as curcumin-binding targets, the expression of which was up-regulated in human leukemia. Curcumin increased ROS levels over the threshold in leukemic cells, and the antioxidant, glutathione (GSH) and overexpression of curcumin-binding enzymes partially mitigated the up-regulation of ROS and growth inhibition caused by curcumin. These results show that curcumin specifically inhibits tumor growth by increasing ROS levels over the threshold through the miscellaneous inhibition of ROS metabolic enzymes. Curcumin has potential in therapy to regulate ROS levels in tumor cells, thereby controlling tumor growth.

Indexed as

Alcohol OxidoreductasesAnimalsAntineoplastic AgentsAntioxidantsCell Line, TumorCell ProliferationCurcuminFemaleGlutathione TransferaseHEK293 CellsHumansMaleMiceMice, NudeNeoplasms, ExperimentalReactive Oxygen SpeciesAlcohol OxidoreductasesAntineoplastic AgentsAntioxidantsCurcuminGlutathione TransferaseReactive Oxygen Species

Identifiers

PMID29391517
PMCPMC5794879
OpenAlexW2802030122

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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.