Evidence map›Paper›PMID 40833485›Full record

ArticleGenes & genomics2025

Targeting the miR-325-3p/GSTP1 axis overcomes paclitaxel resistance in triple-negative breast cancer by inducing ferroptosis.

Huiling Wang, Feng Yang, Yaqin Wu, Zhenyu Zhang, Chaojie Zhang

Abstract read
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In one paragraph

Article in Genes & genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 2 pooled it
–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

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3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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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.

Huiling Wang *Department of Breast and Thyroid Surgery, Hunan Provincial People's Hospital (The First Affiliated Hospital of Hunan Normal University), NO 89, Guhan Road, Changsha, 410006, Hunan, China.
Feng Yang *Department of Pharmacy, Hunan Provincial People's Hospital (The First Affiliated Hospital of Hunan Normal University), Changsha, 410006, Hunan, China.
Yaqin WuDepartment of Breast and Thyroid Surgery, Hunan Provincial People's Hospital (The First Affiliated Hospital of Hunan Normal University), NO 89, Guhan Road, Changsha, 410006, Hunan, China.
Zhenyu ZhangDepartment of Breast and Thyroid Surgery, Hunan Provincial People's Hospital (The First Affiliated Hospital of Hunan Normal University), NO 89, Guhan Road, Changsha, 410006, Hunan, China.
Chaojie ZhangDepartment of Breast and Thyroid Surgery, Hunan Provincial People's Hospital (The First Affiliated Hospital of Hunan Normal University), NO 89, Guhan Road, Changsha, 410006, Hunan, China. zhangchaojie74@126.com.

Funding

Natural Science Foundation of Hunan Province 2022jj30345
6 · The paper itself

Abstract

backgroundTriple-negative breast cancer (TNBC) is an aggressive subtype with limited treatment options, and paclitaxel resistance remains a major therapeutic challenge. Ferroptosis, an iron-dependent cell death mechanism, and microRNAs (miRNAs) like miR-325-3p have emerged as potential regulators of chemoresistance, but their roles in TNBC are poorly understood.

objectiveThis study aimed to investigate whether ferroptosis and miR-325-3p modulate paclitaxel resistance in TNBC and to identify the underlying molecular mechanisms.

methodsPaclitaxel-resistant TNBC cell lines (MDA-MB-231/Pac, SUM159PT/Pac) were established and treated with ferroptosis modulators. miR-325-3p expression was assessed in resistant vs. sensitive TNBC tissues and cells. Functional assays (CCK-8, EdU, flow cytometry, TBARS, FerroOrange) evaluated cell viability, proliferation, apoptosis, and ferroptosis markers. GSTP1 was validated as a miR-325-3p target via dual-luciferase reporter assays and rescue experiments. In vivo xenograft models tested the therapeutic potential of miR-325-3p overexpression with/without GSTP1 restoration.

resultsFerroptosis inducers (erastin, RSL3) sensitized resistant TNBC cells to paclitaxel, while inhibitors (deferiprone, NAC) attenuated this effect. MiR-325-3p was downregulated in paclitaxel-resistant tissues and cells. Its overexpression restored paclitaxel sensitivity by promoting apoptosis and ferroptosis (↑iron accumulation, ↑lipid peroxidation). GSTP1 was identified as a direct target of miR-325-3p. Rescue experiments confirmed that GSTP1 restoration partially reversed miR-325-3p-mediated ferroptosis and paclitaxel sensitization. In vivo, miR-325-3p overexpression suppressed tumor growth, while GSTP1 co-expression mitigated this effect.

conclusionThe miR-325-3p/GSTP1 axis regulates paclitaxel resistance in TNBC by modulating ferroptosis. Targeting this axis represents a promising strategy to overcome chemoresistance.

Indexed as

Drug Resistance, NeoplasmFerroptosisGlutathione S-Transferase piMicroRNAsPaclitaxelTriple Negative Breast NeoplasmsAnimalsApoptosisCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMiceMice, NudeGlutathione S-Transferase piGSTP1 protein, humanMicroRNAsPaclitaxelFerroptosisGSTP1miR-325-3pPaclitaxel resistanceTriple-negative breast cancer (TNBC)

Identifiers

PMID40833485

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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 OpenQuestion graph.