Evidence map›Paper›PMID 38329441›Full record

ArticleAging2024

Mechanism of Erianin anti-triple negative breast cancer based on transcriptomics methods and network pharmacology.

Ming Li, Yuan Zhao, Huimin Li, Shiyao Kang, Xuming Deng, Miaomiao Sheng

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

3 citing papers in PubMed, 2 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
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.

Ming LiLaboratory of Molecular Genetics of Aging and Tumour, Medical School, Kunming University of Science and Technology, Chenggong Campus, Kunming, Yunnan 650500, China.
Yuan ZhaoKunming University of Science and Technology Affiliated Puer City People’s Hospital, Puer, Yunnan 665000, China.
Huimin LiLaboratory of Molecular Genetics of Aging and Tumour, Medical School, Kunming University of Science and Technology, Chenggong Campus, Kunming, Yunnan 650500, China.
Shiyao KangLaboratory of Molecular Genetics of Aging and Tumour, Medical School, Kunming University of Science and Technology, Chenggong Campus, Kunming, Yunnan 650500, China.
Xuming DengLaboratory of Molecular Genetics of Aging and Tumour, Medical School, Kunming University of Science and Technology, Chenggong Campus, Kunming, Yunnan 650500, China.
Miaomiao ShengLaboratory of Molecular Genetics of Aging and Tumour, Medical School, Kunming University of Science and Technology, Chenggong Campus, Kunming, Yunnan 650500, China.
Kunming University of Science and Technology · CNPuer University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Triple negative breast cancer (TNBC) is a highly aggressive illness that lacks effective targeted treatments. Although Erianin has shown potential antitumor properties, its precise mechanism of action and target in TNBC remain unclear, hampering the development of drugs. The present study investigated the underlying mechanism of action of Erianin in treating TNBC by using transcriptomics and network pharmacology approaches. We evaluated Erianin's bioactivity in TNBC cell lines and xenograft tumor models. The results showed that Erianin significantly inhibited TNBC cell proliferation and impeded tumor growth. A subsequent analysis of transcriptomic and network pharmacological data identified 51 mutual targets. Analysis of protein-protein interactions identified eight hub targets. Furthermore, molecular docking indicated that the PPARA binding energy was the lowest for Erianin among the hub targets, followed by ROCK2, PDGFRB, CCND1, MUC1, and CDK1. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes functional enrichment analysis showed that the common targets were associated with multiple cancer-related signaling pathways, including focal adhesion, PI3K-Akt signaling pathway, Rap1 signaling pathway, microRNAs in cancer, and human papillomavirus infection. The results of the Western blot and immunohistochemistry experiment further showed that Erianin could suppress PI3K/Akt signaling pathway activation. After co-incubation with SC79, the cell inhibition rate of Erianin was decreased, which further confirmed that Erianin inhibits TNBC progression via the PI3K-AKT signaling pathway. In conclusion, our results indicated that Erianin has the potential to inhibit the proliferation of TNBC by downregulating the PI3K/AKT signaling pathway by transcriptomics and network pharmacology. Therefore, Erianin appears to be a promising compound for the effective treatment of TNBC.

Indexed as

BibenzylsPhenolTriple Negative Breast NeoplasmsGene Expression ProfilingHumansMolecular Docking SimulationNetwork PharmacologyPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktBibenzylsErianinPhenolPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktErianinmolecular mechanismnetwork pharmacologytranscriptomicstriple-negative breast cancer

Identifiers

PMID38329441
PMCPMC10911376
OpenAlexW4391615751

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.