Evidence map›Paper›PMID 33116405›Full record

ArticleDrug design, development and therapy2020

The Impact of Icariside II on Human Prostate Cancer Cell Proliferation, Mobility, and Autophagy via PI3K-AKT-mTOR Signaling Pathway.

Shuang Li, Yunlu Zhan, Yingwei Xie, Yonghui Wang, Yuexin Liu

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 8% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
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  11. Targeting PI3K/Akt signaling in prostate cancer therapy.Journal of cell communication and signaling · 2023
    Review
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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

5 authors at 1 institution in 1 country.

Shuang Li *Department of Urology, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, People's Republic of China.
Yunlu Zhan *Department of Urology, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, People's Republic of China.ORCID 0000-0003-3744-0846
Yingwei Xie *Department of Urology, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, People's Republic of China.
Yonghui WangDepartment of Urology, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, People's Republic of China.
Yuexin LiuDepartment of Urology, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, People's Republic of China.ORCID 0000-0003-3508-6652
Beijing Tongren Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe flavonol glycoside icariside II (ICA II) has been shown to exhibit a range of anti-tumor properties. Herein, we evaluated the impact of ICA II on human prostate cancer cell proliferation, motility, and autophagy, and we further evaluated the molecular mechanisms underlying these effects.

methodsWe treated DU145 human prostate cancer cells with a range of ICA II doses and then assessed their proliferation via CCK-8 assay, while flow cytometry was used to monitor apoptosis and cell cycle progression. We further utilized wound healing and transwell assays to probe the impact of ICA II on migration and invasion, and assessed autophagy via laser confocal fluorescence microscopy. Western blotting was further utilized to measure LC3-II/I, Beclin-1, P70S6K, PI3K, AKT, mTOR, phospho-AKT, phospho-mTOR, and phospho-P70S6K levels, with qRT-PCR being used to evaluate the expression of specific genes at the mRNA level.

resultsWe found that ICA II was capable of mediating the dose- and time-dependent suppression of DU145 cell proliferation, causing these cells to enter a state of cell cycle arrest and apoptosis. We further determined that ICA II treatment was associated with significant impairment of prostate cancer cell migration and invasion, whereas autophagy was enhanced in treated cells relative to untreated controls.

conclusionOur results indicate that ICA II treatment is capable of suppressing human prostate tumor cell proliferation and migration while enhancing autophagy via modulating the PI3K-AKT-mTOR signaling pathway. As such, ICA II may be an ideal candidate drug for the treatment of prostate cancer.

Indexed as

Antineoplastic Agents, PhytogenicApoptosisAutophagyCell CycleCell Line, TumorCell MovementCell ProliferationDose-Response Relationship, DrugFlavonoidsGene Expression Regulation, NeoplasticHumansMaleOncogene Protein v-aktPhosphatidylinositol 3-KinasesProstatic NeoplasmsSignal TransductionAntineoplastic Agents, Phytogenicbaohuoside IFlavonoidsMTOR protein, humanOncogene Protein v-aktPhosphatidylinositol 3-KinasesTOR Serine-Threonine Kinasesapoptosisautophagyicariside IIPI3K-AKT-mTORprostate cancer

Identifiers

PMID33116405
PMCPMC7549881
OpenAlexW3092392799

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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.