Evidence map›Paper›PMID 31172425›Full record

ArticleBreast cancer (Tokyo, Japan)2019

Icariin induces apoptosis by suppressing autophagy in tamoxifen-resistant breast cancer cell line MCF-7/TAM.

Xia Cheng, Shirui Tan, Feifei Duan, Qingqing Yuan, Qingrong Li, Gang Deng

Open access · hybridAbstract read
In one paragraph

Article in Breast cancer (Tokyo, Japan), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 2 pooled it
7.0field-weighted citation impact, top 3% 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

37 citing papers in PubMed, 2 syntheses or guidelines pooled it, 65 citations in OpenAlex.

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  10. Dual role of autophagy in bone metastasis: mechanistic insights and therapeutic targeting.American journal of clinical and experimental urology · 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

6 authors at 2 institutions in 1 country.

Xia ChengSchool of Agriculture, Yunnan University, Kunming, 650500, Yunnan, China.
Shirui TanSchool of Agriculture, Yunnan University, Kunming, 650500, Yunnan, China.
Feifei DuanSchool of Agriculture, Yunnan University, Kunming, 650500, Yunnan, China.
Qingqing YuanSchool of Agriculture, Yunnan University, Kunming, 650500, Yunnan, China.
Qingrong LiThe Second Affiliated Hospital of Kunming Medical University, Kunming, 650101, Yunnan, China. liqrmed@163.com.
Gang DengSchool of Agriculture, Yunnan University, Kunming, 650500, Yunnan, China. gang_dengGD19@163.com.
Yunnan University · CNKunming Medical University · CN

Funding

National Natural Science Foundation of China 317605403National Natural Science Foundation of Yunnan 2016FB068National Natural Science Foundation of Yunnan 2017FB108
6 · The paper itself

Abstract

backgroundIcariin is a major component isolated from Epimedium brevicornum Maxim and has been reported to exhibit anti-tumor activity. However, whether icariin could reverse the acquired drug resistance in breast cancer remains largely unclear. Therefore, this study was designed to explore the antitumor effects of icariin and its underlying mechanisms in a tamoxifen-resistant breast cancer cell line MCF-7/TAM.

methods3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and Lactate dehydrogenase (LDH) assay were performed to determine the effects of icariin on cell viability and cell death. Cell cycle progression and apoptosis were detected by flow cytometry analysis. Transmission electron microscopy (TEM) assay was utilized to observe cell autophagy. The downstream protein levels were measured using western blotting.

resultsHere, we observed that icariin treatment not only inhibited the growth of MCF-7 but also has a potential function to overcome tamoxifen resistance in MCF-7/TAM. Moreover, icariin significantly induced cell cycle G0/G1 phase arrest and apoptosis, as well as suppressed autophagy. At molecular levels, icariin treatment remarkably down-regulated the expression levels of CDK2, CDK4, Cyclin D1, Bcl-2, LC3-1, LC3-II, AGT5, Beclin-1, but upregulated the expression levels of caspase-3, PARP and p62. Most importantly, we found inhibition of autophagy via 3-MA treatment could significantly enhance the effects of icariin on cell viability and apoptosis. Enhanced autophagy via autophagy related 5 (ATG5) overexpression could partially reverse the effects of icariin on cell viability and apoptosis.

conclusionThese results revealed that icariin might potentially be useful as an adjuvant agent in cancer chemotherapy to enhance the effect of tamoxifen through suppression of autophagy in vitro and provide insight into the therapeutic potential of icariin for the treatment of chemo-resistant breast cancer.

Indexed as

ApoptosisAutophagyAutophagy-Related Protein 5Breast NeoplasmsCaspase 3Cell Cycle CheckpointsCell SurvivalDrug Resistance, NeoplasmEpimediumFemaleFlavonoidsHumansMCF-7 CellsPlant ExtractsPoly(ADP-ribose) PolymerasesProto-Oncogene Proteins c-bcl-2ATG5 protein, humanAutophagy-Related Protein 5BCL2 protein, humanCASP3 protein, humanCaspase 3FlavonoidsicariinPlant ExtractsPoly(ADP-ribose) PolymerasesProto-Oncogene Proteins c-bcl-2Selective Estrogen Receptor ModulatorsTamoxifenApoptosisAutophagyBreast cancerDrug resistanceIcariin

Identifiers

PMID31172425
PMCPMC6821666
OpenAlexW2952081839

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.