Evidence map›Paper›PMID 27329817›Full record

ArticleScientific reports2016

Dioscin strengthens the efficiency of adriamycin in MCF-7 and MCF-7/ADR cells through autophagy induction: More than just down-regulation of MDR1.

Changyuan Wang, Xiaokui Huo, Lijuan Wang, Qiang Meng, Zhihao Liu, Qi Liu, Huijun Sun, Pengyuan Sun, Jinyong Peng, Kexin Liu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 35 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

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 1 institution in 1 country.

Changyuan WangDepartment of Clinical Pharmacology, College of Pharmacy, Dalian Medical University, Dalian, Liaoning, China.
Xiaokui HuoDepartment of Clinical Pharmacology, College of Pharmacy, Dalian Medical University, Dalian, Liaoning, China.
Lijuan WangDepartment of Clinical Pharmacology, College of Pharmacy, Dalian Medical University, Dalian, Liaoning, China.
Qiang MengDepartment of Clinical Pharmacology, College of Pharmacy, Dalian Medical University, Dalian, Liaoning, China.
Zhihao LiuDepartment of Clinical Pharmacology, College of Pharmacy, Dalian Medical University, Dalian, Liaoning, China.
Qi LiuDepartment of Clinical Pharmacology, College of Pharmacy, Dalian Medical University, Dalian, Liaoning, China.
Huijun SunDepartment of Clinical Pharmacology, College of Pharmacy, Dalian Medical University, Dalian, Liaoning, China.
Pengyuan SunDepartment of Clinical Pharmacology, College of Pharmacy, Dalian Medical University, Dalian, Liaoning, China.
Jinyong PengDepartment of Clinical Pharmacology, College of Pharmacy, Dalian Medical University, Dalian, Liaoning, China.
Kexin LiuDepartment of Clinical Pharmacology, College of Pharmacy, Dalian Medical University, Dalian, Liaoning, China.
Dalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The purpose of present study was to investigate the effect of dioscin on activity of adriamycin (ADR) in ADR-sensitive (MCF-7) and ADR-resistant (MCF-7/ADR) human breast cancer cells and to clarify the molecular mechanisms involved. Antiproliferation effect of ADR was enhanced by dioscin in MCF-7 and MCF-7/ADR cells. Dioscin significantly inhibited MDR1 mRNA and protein expression and MDR1 promoter and nuclear factor κ-B (NF-κB) activity in MCF-7/ADR cells. Additionally, inhibitor κB-α (IκB-α) degradation was inhibited by dioscin. Moreover, dioscin induced the formation of vacuoles in the cytoplasm and protein level of LC3-II in MCF-7 and MCF-7/ADR cells. Autophagy inhibitor 3-MA abolished the effect of dioscin on ADR cytotoxicity. Dioscin inhibited phosphorylation of PI3K and Akt, resulting in upregulation of LC3-II expression. In conclusion, dioscin increased ADR chemosensitivity by down-regulating MDR1 expression through NF-κB signaling inhibition in MCF-7/ADR cells. Autophagy was induced by dioscin to ameliorate the cytotoxicity of ADR via inhibition of the PI3K/AKT pathways in MCF-7 and MCF-7/ADR cells. These findings provide evidence in support of further investigation into the clinical application of dioscin as a chemotherapy adjuvant.

Indexed as

AutophagyDown-RegulationATP Binding Cassette Transporter, Subfamily BBreast NeoplasmsCell ProliferationDiosgeninDoxorubicinDrug SynergismFemaleGene Expression Regulation, NeoplasticHumansMCF-7 CellsNF-kappa BPromoter Regions, GeneticSignal TransductionABCB1 protein, humanATP Binding Cassette Transporter, Subfamily BdioscinDiosgeninDoxorubicinNF-kappa B

Identifiers

PMID27329817
PMCPMC4916600
OpenAlexW2460290768

What OpenQuestion holds

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Registered trials

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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.