Evidence map›Paper›PMID 37458908›Full record

ArticleBreast cancer research and treatment2023

FN1 mediated activation of aspartate metabolism promotes the progression of triple-negative and luminal a breast cancer.

Chen Chen, Leiguang Ye, Jinfeng Yi, Tang Liu, Zhigao Li

Erratum issuedAbstract read
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In one paragraph

Article in Breast cancer research and treatment, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

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  5. Developing a gene expression classifier for breast cancer diagnosis.Medical & biological engineering & computing · 2025
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  14. Translational cancer research · 2024
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  16. Targeting RORγ inhibits the growth and metastasis of hepatocellular carcinoma.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Chen Chen *Department of Breast Surgery, Harbin Medical University Cancer Hospital, Harbin, 150081, China.
Leiguang Ye *Department of Respiratory Medicine, Harbin Medical University Cancer Hospital, Harbin, 150081, China.
Jinfeng YiDepartment of Pathology, Harbin Medical University, Harbin, 150081, China.
Tang LiuDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, Harbin, 150081, China. liutang0808@163.com.
Zhigao LiDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, Harbin, 150081, China. drzhigaoli@hrbmu.edu.cn.ORCID http://orcid.org/0000-0002-4169-143X
Harbin Medical University · CN

Funding

National Natural Science Foundation of China 82072903National Natural Science Foundation of China 82073146
6 · The paper itself

Abstract

backgroundBreast cancer (BC) is regarded as one of the most common cancers diagnosed among the female population and has an extremely high mortality rate. It is known that Fibronectin 1 (FN1) drives the occurrence and development of a variety of cancers through metabolic reprogramming. Aspartic acid is considered to be an important substrate for nucleotide synthesis. However, the regulatory mechanism between FN1 and aspartate metabolism is currently unclear.

methodsWe used RNA sequencing (RNA seq) and liquid chromatography-mass spectrometry to analyze the tumor tissues and paracancerous tissues of patients. MCF7 and MDA-MB-231 cells were used to explore the effects of FN1-regulated aspartic acid metabolism on cell survival, invasion, migration and tumor growth. We used PCR, Western blot, immunocytochemistry and immunofluorescence techniques to study it.

resultsWe found that FN1 was highly expressed in tumor tissues, especially in Lumina A and TNBC subtypes, and was associated with poor prognosis. In vivo and in vitro experiments showed that silencing FN1 inhibits the activation of the YAP1/Hippo pathway by enhancing YAP1 phosphorylation, down-regulates SLC1A3-mediated aspartate uptake and utilization by tumor cells, inhibits BC cell proliferation, invasion and migration, and promotes apoptosis. In addition, inhibition of FN1 combined with the YAP1 inhibitor or SLC1A3 inhibitor can effectively inhibit tumor growth, of which inhibition of FN1 combined with the YAP1 inhibitor is more effective.

conclusionTargeting the "FN1/YAP1/SLC1A3/Aspartate metabolism" regulatory axis provides a new target for BC diagnosis and treatment. This study also revealed that intratumoral metabolic heterogeneity plays an important role in the progression of different subtypes of breast cancer.

Indexed as

Breast NeoplasmsTriple Negative Breast NeoplasmsApoptosisAspartic AcidBlotting, WesternCell Line, TumorCell MovementCell ProliferationFemaleFibronectinsGene Expression Regulation, NeoplasticHumansAspartic AcidFibronectinsAspartate metabolismFibronectin 1Metabolic heterogeneityMetabolic reprogramming

Identifiers

PMID37458908
OpenAlexW4384559492

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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.