Evidence map›Paper›PMID 38355608›Full record

ArticleCancer cell international2024

Icariin exerts anti-tumor activity by inducing autophagy via AMPK/mTOR/ULK1 pathway in triple-negative breast cancer.

Mei Zhao, Panling Xu, Wenjing Shi, Juan Wang, Ting Wang, Ping Li

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
7.9field-weighted citation impact, top 2% 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

18 citing papers in PubMed, 17 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Mei Zhao *Department of Chinese Integrative Medicine Oncology, The First Affiliated Hospital of Anhui Medical University, 120 Wanshui Road, Hefei, 230032, Anhui, People's Republic of China.
Panling Xu *Department of Chinese Integrative Medicine Oncology, The First Affiliated Hospital of Anhui Medical University, 120 Wanshui Road, Hefei, 230032, Anhui, People's Republic of China.
Wenjing ShiDepartment of Chinese Integrative Medicine Oncology, The First Affiliated Hospital of Anhui Medical University, 120 Wanshui Road, Hefei, 230032, Anhui, People's Republic of China.
Juan WangDepartment of Chinese Integrative Medicine Oncology, The First Affiliated Hospital of Anhui Medical University, 120 Wanshui Road, Hefei, 230032, Anhui, People's Republic of China.
Ting WangDepartment of Chinese Integrative Medicine Oncology, The First Affiliated Hospital of Anhui Medical University, 120 Wanshui Road, Hefei, 230032, Anhui, People's Republic of China.
Ping LiDepartment of Chinese Integrative Medicine Oncology, The First Affiliated Hospital of Anhui Medical University, 120 Wanshui Road, Hefei, 230032, Anhui, People's Republic of China. liping1964@ahmu.edu.cn.
Anhui Medical University · CNFirst Affiliated Hospital of Anhui Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBreast cancer is the most prevalent female tumor, of which triple-negative breast cancer (TNBC) accounts for about 15%. Characterized by its aggressive nature and limited treatment options, TNBC currently stands as a significant clinical challenge. This study aimed to investigate the effects of icariin (ICA) on TNBC and explore the underlying molecular mechanism.

methodsCell viability was assessed using CCK-8 assay, whereas the impact of ICA on cell proliferation was determined using colony formation assay and detection of proliferating cell nuclear antigen protein. Wound healing and transwell assays were used to evaluate the effects of ICA on cell migration and invasion, respectively. Flow cytometry was used to analyze cell cycle distribution and apoptosis. Transmission electron microscopy and monodansylcaverine staining were performed to detect the induction of autophagy, whereas molecular docking was conducted to predict the potential targets associated with autophagy. The in vivo anti-tumor effects of ICA were evaluated using a TNBC 4T1 xenograft mouse model. Protein expression levels were examined using immunoblotting and immunohistochemistry.

resultsIn vitro, ICA effectively suppressed the viability, proliferation, migration, and invasion of TNBC cells and induced G0/G1 phase cell cycle arrest, apoptosis, and autophagy in TNBC cells by regulating the adenosine monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR)/Unc-51-like kinase 1 (ULK1) signaling pathway. The knockdown of AMPK and inhibition of autophagy with 3-methyladenine reversed the effects of ICA, highlighting the importance of AMPK and autophagy in the anti-cancer mechanism of ICA. In vivo, ICA significantly inhibited TNBC growth, promoted autophagy, and regulated AMPK/mTOR/ULK1 pathway.

conclusionsOur findings demonstrated that ICA exerts anti-cancer effects against TNBC and the associated molecular mechanisms. This study will help to facilitate further preclinical and clinical investigations for the treatment of TNBC.

Indexed as

AMPKApoptosisAutophagyIcariinTNBC

Identifiers

PMID38355608
PMCPMC10868106
OpenAlexW4391831899

What OpenQuestion holds

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LicenceCC BY
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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.