Evidence map›Paper›PMID 35953598›Full record

ArticleOncogene2022

Therapy-induced senescence promotes breast cancer cells plasticity by inducing Lipocalin-2 expression.

Jorge Morales-Valencia, Lena Lau, Teresa Martí-Nin, Ugur Ozerdem, Gregory David

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 34 citations in OpenAlex.

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  14. Therapy-induced senescence in breast cancer: an overview.Exploration of targeted anti-tumor therapy · 2024
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  20. The Potential of Senescence as a Target for Developing Anticancer Therapy.International journal of molecular sciences · 2023
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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

5 authors at 2 institutions in 1 country.

Jorge Morales-Valencia *Department of Biochemistry and Molecular Pharmacology, NYU Langone Medical Center, New York, NY, 10016, USA.
Lena Lau *Department of Biochemistry and Molecular Pharmacology, NYU Langone Medical Center, New York, NY, 10016, USA.
Teresa Martí-NinDepartment of Biochemistry and Molecular Pharmacology, NYU Langone Medical Center, New York, NY, 10016, USA.
Ugur OzerdemDepartment of Pathology, New York University School of Medicine, NYU Langone Health, New York, NY, 10016, USA.
Gregory DavidDepartment of Biochemistry and Molecular Pharmacology, NYU Langone Medical Center, New York, NY, 10016, USA. gregory.david@nyulangone.org.ORCID http://orcid.org/0000-0002-1849-3232
NYU Langone Health · USNew York University · US

Funding

Probing the coordination of cell cycle progression and differentiation in hematopoietic stem cellsR56HL163940 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI DAVID, GREGORY · 2022 to 2022
$539k
Targeting the senescence-associated secretory phenotype as an adjuvant therapy to prevent breast cancer progressionR21CA246416 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI DAVID, GREGORY · 2020 to 2020
$436k
NCI NIH HHS R21 CA246416NHLBI NIH HHS R56 HL163940
6 · The paper itself

Abstract

The acquisition of novel detrimental cellular properties following exposure to cytotoxic drugs leads to aggressive and metastatic tumors that often translates into an incurable disease. While the bulk of the primary tumor is eliminated upon exposure to chemotherapeutic treatment, residual cancer cells and non-transformed cells within the host can engage a stable cell cycle exit program named senescence. Senescent cells secrete a distinct set of pro-inflammatory factors, collectively termed the senescence-associated secretory phenotype (SASP). Upon exposure to the SASP, cancer cells undergo cellular plasticity resulting in increased proliferation, migration and epithelial-to-mesenchymal transition. The molecular mechanisms by which the SASP regulates these pro-tumorigenic features are poorly understood. Here, we report that breast cancer cells exposed to the SASP strongly upregulate Lipocalin-2 (LCN2). Furthermore, we demonstrate that LCN2 is critical for SASP-induced increased migration in breast cancer cells, and its inactivation potentiates the response to chemotherapeutic treatment in mouse models of breast cancer. Finally, we show that neoadjuvant chemotherapy treatment leads to LCN2 upregulation in residual human breast tumors, and correlates with worse overall survival. These findings provide the foundation for targeting LCN2 as an adjuvant therapeutic approach to prevent the emergence of aggressive tumors following chemotherapy.

Indexed as

Breast NeoplasmsAnimalsCarcinogenesisCell CycleCellular SenescenceFemaleHumansLipocalin-2MiceLipocalin-2

Identifiers

PMID35953598
PMCPMC9482949
OpenAlexW4291015544

What OpenQuestion holds

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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.