ORIGINAL RESEARCH article
Front. Mol. Biosci.
Sec. Cellular Biochemistry
This article is part of the Research TopicCell Authentication: Addressing Challenges and FindingsView all 3 articles
Functional and Genomic Characterization of LCN2-Deficient PC-3 Cells Reveals Insights into Prostate Cancer Progression
Provisionally accepted
Kiara Gäberlein1
Diandra Keller2
Sarah K. Schröder-Lange2Phillipp Torkler3
Dominik G. Grimm4Claus Steinlein5
Thomas Haaf1Indrajit Nanda1
Ralf Weiskirchen2*- 1Julius-Maximilians-Universitat Wurzburg, Würzburg, Germany
- 2Institute of Clinical Chemistry and Pathobiochemistry, RWTH Aachen University, Aachen, NRW, Germany
- 3Technische Hochschule Deggendorf, Deggendorf, Germany
- 4Technische Universitat Munchen Campus Straubing fur Biotechnologie und Nachhaltigkeit, Straubing, Germany
- 5Universitatsklinikum Wurzburg, Würzburg, Germany
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Prostate Cancer-3 (PC-3) cells, commonly used as a model for aggressive, androgen-independent prostate cancer, display numerous genetic alterations that contribute to advanced disease, including the loss of tumor suppressors and dysregulated inflammatory signaling. Recent evidence has highlighted the pleiotropic roles of lipocalin 2 (LCN2) in promoting tumor cell proliferation, adhesion, and stress resistance. This study aimed to investigate the functional and molecular effects of LCN2 depletion in PC-3 cells. We conducted a genetic analysis of both the parental PC-3 cell line and a newly created LCN2-deficient PC-3 clone #1 (PC-3 LCN2-KO#1), developed using CRISPR/Cas9 technology. Short tandem repeat (STR) analyses confirmed the authenticity and lineage of each cell line, while next-generation sequencing (NGS) coupled with RT-qPCR validation was used to identify differentially expressed genes and any potential genomic changes resulting from the CRISPR/Cas9 editing process. Our analysis aligned with our previous findings showing that LCN2 is involved in inflammation, endoplasmic reticulum stress responses, and cytoskeletal organization. Previously we have shown that LCN2-deficient cells exhibited decreased invasiveness, disrupted F-actin dynamics, and increased sensitivity to stress-inducing conditions. Consistent with these observations, spectral karyotyping (SKY) and analysis of spontaneously occurring micronuclei revealed an elevated level of chromosomal aberrations in the LCN2-deficient cell line. These results emphasize the significance of LCN2 in driving prostate cancer aggressiveness and provide a foundation for exploring targeted interventions that disrupt LCN2-mediated pathways in advanced disease.
Keywords: Cell culture model, chromosome analysis, CRISPR/Cas9, gene disruption, LCN2, Lipocalins, PC-3, prostate cancer
Received: 23 Oct 2025; Accepted: 03 Feb 2026.
Copyright: © 2026 Gäberlein, Keller, Schröder-Lange, Torkler, Grimm, Steinlein, Haaf, Nanda and Weiskirchen. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Ralf Weiskirchen
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