Evidence map›Paper›PMID 37651362›Full record

ArticleAging2023

Acetyl-cinobufagin suppresses triple-negative breast cancer progression by inhibiting the STAT3 pathway.

Yufeng Qi, Haodong Wu, Tianru Zhu, Zitian Liu, Conghui Liu, Congzhi Yan, Zhixuan Wu, Yiying Xu, Ying Bai, Lehe Yang and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2023. 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
2.9field-weighted citation impact, top 9% 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, 13 citations in OpenAlex.

  1. Article
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  5. Role, mechanisms and effects ofOncology letters · 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

15 authors at 4 institutions in 1 country.

Yufeng QiThe First People’s Hospital of Xiaoshan District, Xiaoshan Affiliated Hospital of Wenzhou Medical University, Hangzhou 311200, Zhejiang, China.
Haodong WuThe First Affiliated Hospital, Wenzhou Medical University, Wenzhou 325000, Zhejiang, China.
Tianru ZhuThe First Affiliated Hospital, Wenzhou Medical University, Wenzhou 325000, Zhejiang, China.
Zitian LiuThe First Affiliated Hospital, Wenzhou Medical University, Wenzhou 325000, Zhejiang, China.
Conghui LiuThe First Affiliated Hospital, Wenzhou Medical University, Wenzhou 325000, Zhejiang, China.
Congzhi YanThe First Affiliated Hospital, Wenzhou Medical University, Wenzhou 325000, Zhejiang, China.
Zhixuan WuThe First Affiliated Hospital, Wenzhou Medical University, Wenzhou 325000, Zhejiang, China.
Yiying XuThe First Affiliated Hospital, Wenzhou Medical University, Wenzhou 325000, Zhejiang, China.
Ying BaiInstitute of Life Sciences, Biomedical Collaborative Innovation Center of Zhejiang Province, Wenzhou University, Wenzhou 325035, Zhejiang, China.
Lehe YangThe First Affiliated Hospital, Wenzhou Medical University, Wenzhou 325000, Zhejiang, China.
Dezhi ChengThe First Affiliated Hospital, Wenzhou Medical University, Wenzhou 325000, Zhejiang, China.
Xiaohua ZhangThe First Affiliated Hospital, Wenzhou Medical University, Wenzhou 325000, Zhejiang, China.
Haiyang ZhaoInstitute of Life Sciences, Biomedical Collaborative Innovation Center of Zhejiang Province, Wenzhou University, Wenzhou 325035, Zhejiang, China.
Chengguang ZhaoThe First Affiliated Hospital, Wenzhou Medical University, Wenzhou 325000, Zhejiang, China.
Xuanxuan DaiThe First Affiliated Hospital, Wenzhou Medical University, Wenzhou 325000, Zhejiang, China.
Wenzhou Medical University · CNFirst Affiliated Hospital of Wenzhou Medical University · CNWenzhou University · CNThe First People's Hospital of Xiaoshan District, Hangzhou · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe incidence of breast cancer (BC) worldwide has increased substantially in recent years. Epithelial-mesenchymal transition (EMT) refers to a crucial event impacting tumor heterogeneity. Although cinobufagin acts as an effective anticancer agent, the clinical use of cinobufagin is limited due to its strong toxicity. Acetyl-cinobufagin, a pre-drug of cinobufagin, was developed and prepared with greater efficacy and lower toxicity.

methodsA heterograft mouse model using triple negative breast cancer (TNBC) cell lines, was used to evaluate the potency of acetyl-cinobufagin. Signal transducer and stimulator of transcription 3 (STAT3)/EMT involvement was investigated by gene knockout experiments using siRNA and Western blot analysis.

resultsAcetyl-cinobufagin inhibited proliferation, migration, and cell cycle S/G2 transition and promoted apoptosis in TNBC cells

conclusionsThe findings of this study support the potential clinical use of acetyl-cinobufagin as a STAT3 inhibitor in TNBC adjuvant therapy.

Indexed as

BufanolidesTriple Negative Breast NeoplasmsAnimalsDisease Models, AnimalHumansInterleukin-6MicePhosphorylationSTAT3 Transcription FactorBufanolidescinobufaginInterleukin-6STAT3 protein, humanSTAT3 Transcription Factoracetyl-cinobufaginepithelial-mesenchymal transitionSTAT3STAT3 inhibitortriple negative breast cancer

Identifiers

PMID37651362
PMCPMC10497018
OpenAlexW4386323255

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.