Evidence map›Paper›PMID 34826043›Full record

ArticleChinese journal of integrative medicine2022

Bufalin Induces Programmed Necroptosis in Triple-Negative Breast Cancer Drug-Resistant Cell Lines through RIP1/ROS-Mediated Pathway.

Xiao-Dan Liu, Cheng-Yang Song, Cui-Cui Kong, Xin Tian

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Article in Chinese journal of integrative medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

10 citing papers in PubMed, 19 citations in OpenAlex.

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  6. The Role of Redox Environment in Tumors.Current medicinal chemistry · 2025
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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

4 authors at 2 institutions in 1 country.

Xiao-Dan LiuDepartment of Breast Surgery, the Fourth Affiliated Hospital of China Medical University, Shenyang, 110032, China.
Cheng-Yang SongDepartment of Thoracic Surgery, the Fourth Affiliated Hospital of China Medical University, Shenyang, 110032, China.
Cui-Cui KongMolecular Oncology Laboratory of Cancer Research Institute, the First Affiliated Hospital of China Medical University, Shenyang, 110001, China.
Xin TianMolecular Oncology Laboratory of Cancer Research Institute, the First Affiliated Hospital of China Medical University, Shenyang, 110001, China. tianxin@cmu1h.com.
China Medical University · CNFourth Affiliated Hospital of China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo explore the effect and mechanism of action of bufalin in triple-negative breast cancer (TNBC) drug-resistant cell lines.

methodsThe normal human mammary epithelial cell line, TNBC cell line, TNBC adriamycin-resistant cell line, and TNBC docetaxel-resistant cell line were treated with different doses of bufalin (0-1,000 nmol/L) at different time points (0-72 h). Propidium iodide staining, AV-FITC/PI double staining, Hoechst 33342/PI double staining and transmission electron microscopy (TEM) were used to evaluate the death patterns of the cell lines.

resultsBufalin killed the TNBC cell line and its drug-resistant cell lines in a dose/time-dependent manner (all P<0.01). After treatment with bufalin for 24 h, the adriamycin-resistant cell line showed a co-existing pattern of necroptosis and apoptosis. However, at 48 h, necroptosis was the main manifestation. After treatment with bufalin, the expressions of tumor necrosis factor α, phospho-tumor necrosis factor receptor 1, phospho-receptor interacting protein 1 and c-caspase 3 increased (all P<0.01), the killing effect of bufalin could be mostly inhibited by NEC-1, and by z-VAD-fmk (both P<0.01). Besides, the intracellular reactive oxygen species (ROS) levels increased considerably (P<0.01), the antioxidant N-acetyl cysteine or Nec-1 could inhibit the increase of ROS level and the killing effect of bufalin (all P<0.01). The adriamycin-resistant cell line exhibited necroptosis characteristic after 48 h of bufalin treatment under TEM.

conclusionsBufalin could induce necroptosis through RIP1/ROS-mediated pathway to kill the drug-resistant TNBC cell lines. This finding provides critical experimental data and theoretical basis for the clinical application of bufalin to overcome the difficulties in the treatment of TNBC.

Indexed as

NecroptosisTriple Negative Breast NeoplasmsAntioxidantsApoptosisBufanolidesCaspase 3Cell LineCell Line, TumorCysteineDocetaxelDoxorubicinFluorescein-5-isothiocyanateHumansPropidiumReactive Oxygen SpeciesReceptors, Tumor Necrosis FactorAntioxidantsbufalinBufanolidesCaspase 3CysteineDocetaxelDoxorubicinFluorescein-5-isothiocyanatePropidiumReactive Oxygen SpeciesReceptors, Tumor Necrosis FactorTumor Necrosis Factor-alphabufalindrug resistantnecroptosisreactive oxygen species pathwaytriple-negative breast cancer

Identifiers

PMID34826043
OpenAlexW3215038008

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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 OpenQuestion graph.