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

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A Correction to this article was published on 28 December 2023

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Abstract

Background

Breast 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.

Methods

We 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.

Results

We 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.

Conclusion

Targeting 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.

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Data availability

The RNA-seq data have been deposited in the NCBI GEO under accession number PRJNA962803, and the metabolomics data in this study can be obtained from the corresponding author on request.

Change history

Abbreviations

Asp:

Aspartate

BC:

Breast cancer

CCK-8:

Cell Counting Kit-8

Co-IP:

Co-immunoprecipitation

CRC:

Colorectal cancer

EAAT1:

Excitatory amino acid transporter 1

ECM:

Extracellular matrix

FBS:

Fetal bovine serum

FDR:

False discovery rate

FN:

Fibronectin

GLAST:

Glutamate/aspartate transporter

GO:

Gene ontology

HCA:

Hierarchical cluster analysis

IF:

Immunofluorescence staining

IHC:

Immunohistochemistry

KEGG:

Kyoto Encyclopedia of Genes and Genomes

LC–MS:

Liquid chromatography–mass spectrometry

NCCR:

National Central Cancer Registry

OSR:

Overall survival rate

qRT-PCR:

Reverse Transcriptase qPCR

Q-TOF MS:

Quadrupole time-of-flight mass spectrometer

RNA seq:

RNA sequencing

SLC:

Solute carrier family

SLC1A3:

Solute carrier family 1 member 3

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Acknowledgements

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Funding

This study was supported by National Natural Science Foundation of China (82073146 and 82072903).

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Author notes

  1. Chen Chen and Leiguang Ye have contributed equally to this work and share first authorship. Zhigao Li and Tong Liu are co corresponding authors.

Authors and Affiliations

  1. Department of Breast Surgery, Harbin Medical University Cancer Hospital, Harbin, 150081, China

    Chen Chen, Tang Liu & Zhigao Li

  2. Department of Respiratory Medicine, Harbin Medical University Cancer Hospital, Harbin, 150081, China

    Leiguang Ye

  3. Department of Pathology, Harbin Medical University, Harbin, 150081, China

    Jinfeng Yi

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Contributions

CC and LY conceived the study, did the experiment, analyzed the data and writing the manuscript; JY analyzed and proofread the data; ZL and TL supervised the study. All authors read and approved the final manuscript.

Corresponding authors

Correspondence to Tang Liu or Zhigao Li.

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The authors declare that they have no conflicts of interest.

Ethical approval

All experimental protocols were approved by the Animal Ethics Committee of Harbin Medical University Cancer Hospital. All methods were carried out in accordance with the Guide for the Care and Use of Laboratory Animals. All methods are reported in accordance with ARRIVE guidelines for the reporting of animal experiments. The study was carried out in accordance with the relevant guidelines and regulation.

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Informed consent was obtained from all subjects prior to collection and all samples were subjected to histological confirmation. The study was conducted in accordance with the Declaration of Helsinki.

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In the original publication of the article, the name and email address of the first corresponding author was published incorrectly as Tong Liu, liutong@hrbmu.edu.cn. The corrected name should read as Tang Liu and the corrected email address should read as liutang0808@163.com. Also, the layout ratio was incorrect in Fig. 4. The corrected Fig. 4 is provided below.

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Chen, C., Ye, L., Yi, J. et al. FN1 mediated activation of aspartate metabolism promotes the progression of triple-negative and luminal a breast cancer. Breast Cancer Res Treat 201, 515–533 (2023). https://doi.org/10.1007/s10549-023-07032-9

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