Evidence map›Paper›PMID 30710454›Full record

ArticleBritish journal of pharmacology2019

Potent effects of dioscin against hepatocellular carcinoma through regulating TP53-induced glycolysis and apoptosis regulator (TIGAR)-mediated apoptosis, autophagy, and DNA damage.

Zhang Mao, Xu Han, Dahong Chen, Youwei Xu, Lina Xu, Lianhong Yin, Huijun Sun, Yan Qi, Lingling Fang, Kexin Liu and 1 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2019. 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 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

32 citing papers in PubMed, 58 citations in OpenAlex.

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  4. The anti-cancer activity of Dioscin: an update and future perspective.Medical oncology (Northwood, London, England) · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 1 institution in 1 country.

Zhang MaoCollege of Pharmacy, Dalian Medical University, Dalian, China.
Xu HanCollege of Pharmacy, Dalian Medical University, Dalian, China.
Dahong ChenCollege of Pharmacy, Dalian Medical University, Dalian, China.
Youwei XuCollege of Pharmacy, Dalian Medical University, Dalian, China.
Lina XuCollege of Pharmacy, Dalian Medical University, Dalian, China.
Lianhong YinCollege of Pharmacy, Dalian Medical University, Dalian, China.
Huijun SunCollege of Pharmacy, Dalian Medical University, Dalian, China.
Yan QiCollege of Pharmacy, Dalian Medical University, Dalian, China.
Lingling FangCollege of Pharmacy, Dalian Medical University, Dalian, China.
Kexin LiuCollege of Pharmacy, Dalian Medical University, Dalian, China.
Jinyong PengCollege of Pharmacy, Dalian Medical University, Dalian, China.ORCID 0000-0002-6265-2667
Dalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeDioscin shows potent effects against cancers. We aimed to elucidate its pharmacological effects and mechanisms of action on hepatocellular carcinoma (HCC) in vivo and in vitro. EXPERIMENTAL APPROACH: Effects of dioscin were investigated in SMMC7721 and HepG2 cells, diethylnitrosamine-induced primary liver cancer in rats, and cell xenografts in nude mice. Isobaric tags for relative and absolution quantitation (iTRAQ)-based proteomics was used to find dioscin's targets and investigate its mechanism. KEY

resultsIn SMMC7721 and HepG2 cells dioscin markedly inhibited cell proliferation and migration, induced apoptosis, autophagy, and DNA damage. It inhibited DEN-induced primary liver cancer in rats, markedly changed body weights and restored levels of α fetoprotein, alanine transaminase, aspartate transaminase, γ-glutamyltransferase, alkaline phosphatase, and Ki67. It also inhibited growth of xenografts in mice. In SMMC7721 cells, 191 differentially expressed proteins were found after dioscin, based on iTRAQ-based assay. TP53-inducible glycolysis and apoptosis regulator (TIGAR) was identified as being significantly down-regulated by dioscin. Dioscin induced cell apoptosis, autophagy, and DNA damage via increasing expression levels of p53, cleaved PARP, Bax, cleaved caspase-3/9, Beclin-1, and LC3 and suppressing those of Bcl-2, p-Akt, p-mammalian target of rapamycin (mTOR), CDK5, p-ataxia telangiectasia-mutated gene (ATM). The transfection of TIGAR siRNA into SMMC7721 cells and xenografts in nude mice further confirmed that the potent activity of dioscin against HCC is evoked by adjusting TIGAR-mediated inhibition of p53, Akt/mTOR, and CDK5/ATM pathways. CONCLUSIONS AND IMPLICATIONS: The data suggest that dioscin has potential as a therapeutic, and TIGAR as a drug target for treating HCC.

Indexed as

AnimalsAntineoplastic AgentsApoptosisApoptosis Regulatory ProteinsAutophagyCarcinoma, HepatocellularCell LineCell SurvivalDiosgeninDNA DamageGlycolysisHumansLiver NeoplasmsMaleMice, Inbred BALB CMice, NudeAntineoplastic AgentsApoptosis Regulatory ProteinsdioscinDiosgeninPhosphoric Monoester HydrolasesRNA, Small InterferingTumor Suppressor Protein p53

Identifiers

PMID30710454
PMCPMC6433650
OpenAlexW2914380791

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.