Evidence map›Paper›PMID 29614812›Full record

ArticleInternational journal of molecular sciences2018

20(S)-Protopanaxadiol-Induced Apoptosis in MCF-7 Breast Cancer Cell Line through the Inhibition of PI3K/AKT/mTOR Signaling Pathway.

Hong Zhang, Hua-Li Xu, Yu-Chen Wang, Ze-Yuan Lu, Xiao-Feng Yu, Da-Yun Sui

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 46 citations in OpenAlex.

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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 1 institution in 1 country.

Hong ZhangDepartment of Pharmacology, School of Pharmaceutical Sciences, Jilin University, Changchun 130021, China. zlzhoan@163.com.
Hua-Li XuDepartment of Pharmacology, School of Pharmaceutical Sciences, Jilin University, Changchun 130021, China. xhl@jlu.edu.cn.
Yu-Chen WangDepartment of Pharmacology, School of Pharmaceutical Sciences, Jilin University, Changchun 130021, China. scarwyc@163.com.ORCID 0000-0002-6064-9480
Ze-Yuan LuDepartment of Pharmacology, School of Pharmaceutical Sciences, Jilin University, Changchun 130021, China. zeyuanlu@jlu.edu.cn.
Xiao-Feng YuDepartment of Pharmacology, School of Pharmaceutical Sciences, Jilin University, Changchun 130021, China. xiaofengyu1962@163.com.
Da-Yun SuiDepartment of Pharmacology, School of Pharmaceutical Sciences, Jilin University, Changchun 130021, China. suidy@jlu.edu.cn.
Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

20(S)-Protopanaxadiol (PPD) is one of the major active metabolites of ginseng. It has been reported that 20(S)-PPD shows a broad spectrum of antitumor effects. Our research study aims were to investigate whether apoptosis of human breast cancer MCF-7 cells could be induced by 20(S)-PPD by targeting the Phosphatidylinositol 3-kinase/Protein kinase B/Mammalian target of rapamycin (PI3K/AKT/mTOR) signal pathway in vitro and in vivo. Cell cycle analysis was performed by Propidium Iodide (PI) staining. To overexpress and knock down the expression of mTOR, pcDNA3.1-mTOR and mTOR small interfering RNA (siRNA) transient transfection assays were used, respectively. Cell viability and apoptosis were evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT)-test and Annexin V /PI double-staining after transfection. The antitumor effect in vivo was determined by the nude mice xenograft assay. After 24 h of incubation, treatment with 20(S)-PPD could upregulate phosphorylated-Phosphatase and tensin homologue deleted on chromosome 10 (p-PTEN) expression and downregulate PI3K/AKT/mTOR-pathway protein expression. Moreover, G0/G1 cell cycle arrest in MCF-7 cells could be induced by 20(S)-PPD treatment at high concentrations. Furthermore, overexpression or knockdown of mTOR could inhibit or promote the apoptotic effects of 20(S)-PPD. In addition, tumor volumes were partially reduced by 20(S)-PPD at 100 mg/kg in a MCF-7 xenograft model. Immunohistochemical staining indicated a close relationship between the inhibition of tumor growth and the PI3K/AKT/mTOR signal pathway. PI3K/AKT/mTOR pathway-mediated apoptosis may be one of the potential mechanisms of 20(S)-PPD treatment.

Indexed as

ApoptosisCell Line, TumorFemaleHumansMCF-7 CellsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSapogeninsSignal TransductionTOR Serine-Threonine KinasesMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktprotopanaxadiolSapogeninsTOR Serine-Threonine Kinases20(S)-ProtopanaxadiolapoptosisMCF-7PI3K/AKT/mTOR

Identifiers

PMID29614812
PMCPMC5979555
OpenAlexW2794610215

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.