Evidence map›Paper›PMID 27791197›Full record

ArticleOncotarget2016

Epigallocatechin-3-gallate(EGCG) suppresses melanoma cell growth and metastasis by targeting TRAF6 activity.

Jianglin Zhang, Zhou Lei, Zunnan Huang, Xu Zhang, Youyou Zhou, Zhongling Luo, Weiqi Zeng, Juan Su, Cong Peng, Xiang Chen

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
6.9field-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

52 citing papers in PubMed, 84 citations in OpenAlex.

  1. Review
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  6. Green Tea Catechins and Skin Health.Antioxidants (Basel, Switzerland) · 2024
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  20. An update on clinical trials for chemoprevention of human skin cancer.Journal of cancer metastasis and treatment · 2023
    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

10 authors at 3 institutions in 1 country.

Jianglin ZhangThe Department of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Zhou LeiThe Department of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Zunnan HuangKey Laboratory for Medical Molecular Diagnostics of Guangdong Province, Dongguan Scientific Research Center, Guangdong Medical University, Dongguan, Guangdong, China.
Xu ZhangThe Department of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Youyou ZhouThe Department of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Zhongling LuoThe Department of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Weiqi ZengThe Department of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Juan SuThe Department of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Cong PengThe Department of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Xiang ChenThe Department of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Xiangya Hospital Central South University · CNCentral South University · CNGuangdong Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TRAF6 (TNF Receptor-Associated Factor 6) is an E3 ubiquitin ligase that contains a Ring domain, induces K63-linked polyubiquitination, and plays a critical role in signaling transduction. Our previous results demonstrated that TRAF6 is overexpressed in melanoma and that TRAF6 knockdown dramatically attenuates tumor cell growth and metastasis. In this study, we found that EGCG can directly bind to TRAF6, and a computational model of the interaction between EGCG and TRAF6 revealed that EGCG probably interacts with TRAF6 at the residues of Gln54, Gly55, Asp57 ILe72, Cys73 and Lys96. Among these amino acids, mutation of Gln54, Asp57, ILe72 in TRAF6 could destroy EGCG bound to TRAF6, furthermore, our results demonstrated that EGCG significantly attenuates interaction between TRAF6 and UBC13(E2) and suppresses TRAF6 E3 ubiquitin ligase activity in vivo and in vitro. Additionally, the phosphorylation of IκBα, p-TAK1 expression are decreased and the nuclear translocation of p65 and p50 is blocked by treatment with EGCG, leading to inactivation of the NF-κB pathway. Moreover, EGCG significantly inhibits cell growth as well as the migration and invasion of melanoma cells. Taken together, these findings show that EGCG is a novel E3 ubiquitin ligase inhibitor that could be used to target TRAF6 for chemotherapy or the prevention of melanoma.

Indexed as

AnimalsAntineoplastic Agents, PhytogenicCatechinCell Line, TumorCell MovementCell ProliferationEnzyme InhibitorsGene Expression Regulation, NeoplasticHEK293 CellsHumansIntracellular Signaling Peptides and ProteinsLung NeoplasmsMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMelanomaMice, Inbred BALB CAntineoplastic Agents, PhytogenicCatechinEnzyme Inhibitorsepigallocatechin gallateIntracellular Signaling Peptides and ProteinsMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesNF-kappa BNF-KappaB Inhibitor alphaNFKBIA protein, humanTifab protein, humanTNF Receptor-Associated Factor 6UBE2N protein, humanUbiquitin-Conjugating EnzymesUbiquitin-Protein LigasesEGCGmelanomaTRAF6ubiquitination

Identifiers

PMID27791197
PMCPMC5346735
OpenAlexW2535162854

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.