Evidence map›Paper›PMID 40708058›Full record

ArticleHereditas2025

The potential mechanism of Saikosaponin D against luminal A breast cancer based on bioinformatical analysis, molecular docking and in vitro studies.

Lichang Yang, Ru Chang, Jianzhen Pan, Shan Huang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Hereditas, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
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

4 authors.

Lichang YangAnhui University of Chinese Medicine, Hefei, 230012, China.
Ru ChangDepartment of Oncology, The First Affiliated Hospital of Harbin Medical University, Harbin, 150001, China.
Jianzhen PanDepartment of Intensive Care Medicine, Hunan Cancer Hospital, The Affiliated Cancer Hospital of Xiangya School of Medicine Central South University, Changsha, 410003, China.
Shan HuangChongqing Medical and Pharmaceutical College, No.82, Daxuecheng Middle Road, Shapingba District, Chongqing, 401331, China. huangshancq1983@163.com.

Funding

A Construction Project of the Key Laboratory of Chongqing Medical and Pharmaceutical College ygz2021501Science and Technology Research Project of Chongqing Education Commission KJQN202202827、KJQN202402834the fifth batch of Chinese National Excellent Clinical Talents Training Program of the State Administration of Traditional Chinese Medicine (National Traditional Chinese Medicine Education Letter） [2022] No. 239Tianhan Zhou National Famous Traditional Chinese Medicine Inheritance Studio Construction Project (National Traditional Chinese Medicine Education Letter） [2022] No. 245
6 · The paper itself

Abstract

backgroundSaikosaponin D (SSD) has been shown to have the strongest anti-tumor activity. This study aimed to explore the effects and potential molecular mechanism of Saikosaponin D (SSD) against estrogen receptor-positive breast cancer.

methodsMCF-7 and T-47D cell lines were treated with a series of concentrations of SSD. Growth, cell cycle distribution, and apoptosis tests were performed. Next, potential targets of SSD against breast cancer were predicted. The targets for SSD were collected from HERB database and PharmMapper Server and displayed accoding to degree.

resultsthere was a dose-dependent decrease in MCF-7 and T-47D cancer cell viability and the the half maximal inhibitory concentrations were 7.31 ± 0.63 µM and 9.06 ± 0.45 µM, respectively. Treatment with SSD decreased cell proliferation, arrested cell cycle at G1, and induced cell apoptosis. There were 227 potential targets of SSD against breast cancer, among which ESR1 was a hub gene. SSD treatment can reduce the protein levels of estrogen receptor α (ERα), Cyclin D1 (CCND1), and the proto-oncogene c-Myc (c-Myc).

conclusionSSD may have therapeutic potential in estrogen receptor-positive breast cancer, may through its suppression on ESR1.

Indexed as

Antineoplastic AgentsBreast NeoplasmsOleanolic AcidSaponinsApoptosisCell Line, TumorCell ProliferationCell SurvivalComputational BiologyEstrogen Receptor alphaFemaleHumansMCF-7 CellsMolecular Docking SimulationProto-Oncogene MasAntineoplastic AgentsESR1 protein, humanEstrogen Receptor alphaMAS1 protein, humanOleanolic AcidProto-Oncogene Massaikosaponin DSaponinsBreast cancerCell cycleEstrogen receptorProliferationSaikosaponin D

Identifiers

PMID40708058
PMCPMC12291396

What OpenQuestion holds

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LicenceCC BY
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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.