Evidence mapPaperPMID 40076939Full record

ArticleInternational journal of molecular sciences2025

Kinsenoside Suppresses DGAT1-Mediated Lipid Droplet Formation to Trigger Ferroptosis in Triple-Negative Breast Cancer.

Yaqin Yang, Dandan Chen, Yuru Zhu, Min Zhang, Huajun Zhao

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

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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

4 citing papers in PubMed.

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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.

Yaqin YangSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou 311402, China.
Dandan ChenSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou 311402, China.
Yuru ZhuSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou 311402, China.
Min ZhangSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou 311402, China.
Huajun ZhaoSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou 311402, China.

Funding

Key Research Project of Traditional Chinese Medicine in Zhejiang Province 2022ZZ008National Natural Science Foundation of China 82474271
6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) presents limited therapeutic options and is characterized by a poor prognosis. Although Kinsenoside (KIN) possesses a wide range of pharmacological activities, its effect and mechanism in TNBC remain unclear. The objective of this research was to explore the therapeutic effectiveness and the molecular mechanisms of KIN on TNBC. Xenograft experiment was carried out to assess the impact of KIN on TNBC in vivo. The effect of KIN on TNBC in vitro was evaluated through the analysis of cell cytotoxicity and colony formation assays. Oil Red O staining and BODIPY 493/503 fluorescence staining were employed to detect the effect of KIN on lipid droplet (LD) formation. Transcriptomics and inhibitor-rescue experiments were conducted to investigate the role of KIN on TNBC. Mechanistic experiments, including quantitative real-time polymerase chain reaction (RT-qPCR), Western blotting, diacylglycerol acyltransferase 1 (DGAT1) overexpression assay, and flow cytometric assay, were employed to uncover the regulatory mechanisms of KIN on TNBC. KIN inhibited tumor growth without causing obvious toxicity to the liver and kidneys. In vitro experiments demonstrated that KIN significantly inhibited the viability and proliferation of TNBC cells, accompanied by decreased LD formation and lipid content. Polyunsaturated fatty acids (PUFAs) levels were significantly increased by KIN. Furthermore, transcriptomics and inhibitor-rescue experiments revealed that KIN induced ferroptosis in TNBC cells. KIN could significantly regulate ferroptosis-related proteins. Lipid peroxidation, iron accumulation, and GSH depletion also confirmed this. The LD inducer mitigated the KIN-induced ferroptosis in TNBC. The overexpression of DGAT1 attenuated the effects of KIN on cell viability and proliferation. Furthermore, the overexpression of DGAT1 inhibited the effect of KIN to trigger ferroptosis in TNBC cells. Our findings confirmed that KIN could trigger ferroptosis by suppressing DGAT1-mediated LD formation, thereby demonstrating a promising therapeutic effect of KIN in TNBC.

Indexed as

4-ButyrolactoneDiacylglycerol O-AcyltransferaseFerroptosisLipid DropletsTriple Negative Breast NeoplasmsAnimalsCell Line, TumorCell ProliferationCell SurvivalFemaleGene Expression Regulation, NeoplasticHumansMiceMice, Inbred BALB CMice, NudeXenograft Model Antitumor Assays4-ButyrolactoneDGAT1 protein, humanDiacylglycerol O-AcyltransferaseDGAT1ferroptosiskinsenosidelipid droplet formationtriple-negative breast cancer

Identifiers

PMID40076939
PMCPMC11900917

What Socratic holds

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Registered trials

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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 Socratic graph.