Evidence map›Paper›PMID 29024409›Full record

ArticleJournal of cellular and molecular medicine2018

The natural agent rhein induces β-catenin degradation and tumour growth arrest.

Shu Liu, Jiao Wang, Ting Shao, Peiying Song, Qingbin Kong, Hui Hua, Ting Luo, Yangfu Jiang

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.1field-weighted citation impact, top 27% 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

18 citing papers in PubMed, 21 citations in OpenAlex.

  1. Rhein and its derivatives: potential anti-tumor drugs and corresponding targeted mechanism.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Shu LiuState Key Laboratory of Biotherapy, Section of Oncogene, Cancer Center, West China Hospital, Sichuan University, Chengdu, China.
Jiao WangSchool of Basic Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Ting ShaoState Key Laboratory of Biotherapy, Section of Oncogene, Cancer Center, West China Hospital, Sichuan University, Chengdu, China.
Peiying SongState Key Laboratory of Biotherapy, Section of Oncogene, Cancer Center, West China Hospital, Sichuan University, Chengdu, China.
Qingbin KongState Key Laboratory of Biotherapy, Section of Oncogene, Cancer Center, West China Hospital, Sichuan University, Chengdu, China.
Hui HuaLaboratory of Stem Cell Biology, West China Hospital, Sichuan University, Chengdu, China.
Ting LuoCancer Center, West China Hospital, Chengdu, China.
Yangfu JiangState Key Laboratory of Biotherapy, Section of Oncogene, Cancer Center, West China Hospital, Sichuan University, Chengdu, China.ORCID 0000-0002-8696-2651
Sichuan University · CNChengdu University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The natural agent rhein is an ananthraquinone derivative of rhubarb, which has anticancer effects. To determine the mechanisms underlying the anticancer effects of rhein, we detected the effect of rhein on several oncoproteins. Here, we show that rhein induces β-catenin degradation in both hepatoma cell HepG2 and cervical cancer cell Hela. Treatment of HepG2 and Hela cells with rhein shortens the half-life of β-catenin. The proteasome inhibitor MG132 blunts the downregulation of β-catenin by rhein. The induction of β-catenin degradation by rhein is dependent on GSK3 but independent of Akt. Treatment of HepG2 and Hela cells with GSK3 inhibitor or GSK3β knockdown abrogates the effect of rhein on β-catenin. GSK3β knockdown compromises the inhibition of HepG2 and Hela cell growth by rhein. Furthermore, rhein dose not downregulate β-catenin mutant that is deficient of phosphorylation at multiple residues including Ser33, Ser37, Thr41 and Ser45. Moreover, rhein induces cell cycle arrest at S phase in both HepG2 and Hela cells. Intraperitoneal administration of rhein suppresses tumour cells proliferation and tumour growth in HepG2 xenografts model. Finally, the levels of β-catenin are reduced in rhein-treated tumours. These data demonstrate that rhein can induce β-catenin degradation and inhibit tumour growth.

Indexed as

AnimalsAnthraquinonesAntineoplastic Agentsbeta CateninBiological ProductsCell Cycle CheckpointsCell ProliferationFemaleGlycogen Synthase Kinase 3 betaHeLa CellsHep G2 CellsHumansMice, Inbred BALB CMice, NudeNeoplasm ProteinsNeoplasmsAnthraquinonesAntineoplastic Agentsbeta CateninBiological ProductsGlycogen Synthase Kinase 3 betaNeoplasm ProteinsProteasome Endopeptidase ComplexProto-Oncogene Proteins c-aktrheinRNA, Messengercancer therapyNatural productrheinβ-catenin

Identifiers

PMID29024409
PMCPMC5742736
OpenAlexW2763361919

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.