ArticleBreast cancer research : BCR2013
LOXL2 induces aberrant acinar morphogenesis via ErbB2 signaling.
Article in Breast cancer research : BCR, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 37 citations in OpenAlex.
- Systematic Characterisation and Analysis of Lysyl Oxidase Family Members as Drivers of Tumour Progression and Multiple Drug Resistance.Journal of cellular and molecular medicine · 2025Article
- siLOXL2 Inhibits Endothelial Inflammatory Response and EndMT Induced by ox-LDL.Cerebrovascular diseases extra · 2024Article
- Lysyl Oxidase (LOX) Family Proteins: Key Players in Breast Cancer Occurrence and Progression.Journal of Cancer · 2024Review
- Lysyl oxidase-like 2 promotes stemness and enhances antitumor effects of gefitinib in head and neck cancer via IFIT1 and IFIT3.Cancer science · 2023Article
- LOXL2 in Cancer: A Two-Decade Perspective.International journal of molecular sciences · 2023Review
- LOX overexpression programming mediates the osteoclast mechanism of low peak bone mass in female offspring rats caused by pregnant dexamethasone exposure.Cell communication and signaling : CCS · 2023Article
- Lysyl oxidase-like 2 processing by factor Xa modulates its activity and substrate preference.Communications biology · 2023Article
- Lysyl Oxidase Family Proteins: Prospective Therapeutic Targets in Cancer.International journal of molecular sciences · 2022Review
- GDNF Promotes Astrocyte Abnormal Proliferation and Migration Through the GFRα1/RET/MAPK/pCREB/LOXL2 Signaling Axis.Molecular neurobiology · 2022Article
- Lysyl oxidase-like 2 inhibitor rescues D-galactose-induced skeletal muscle fibrosis.Aging cell · 2022Article
- Lysyl oxidases: linking structures and immunity in the tumor microenvironment.Cancer immunology, immunotherapy : CII · 2020Review
- Review
- Lysyl oxidase-like 2 is a regulator of angiogenesis through modulation of endothelial-to-mesenchymal transition.Journal of cellular physiology · 2019Article
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- Human lysyl oxidase-like 2.Bioorganic chemistry · 2014Review
- When Good Turns Bad: Regulation of Invasion and Metastasis by ErbB2 Receptor Tyrosine Kinase.Cells · 2014Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 5 countries.
Funding
Abstract
introductionLysyl oxidase-like 2 (LOXL2) is a matrix-remodeling enzyme that has been shown to play a key role in invasion and metastasis of breast carcinoma cells. However, very little is known about its role in normal tissue homeostasis. Here, we investigated the effects of LOXL2 expression in normal mammary epithelial cells to gain insight into how LOXL2 mediates cancer progression.
methodsLOXL2 was expressed in MCF10A normal human mammary epithelial cells. The 3D acinar morphogenesis of these cells was assessed, as well as the ability of the cells to form branching structures on extracellular matrix (ECM)-coated surfaces. Transwell-invasion assays were used to assess the invasive properties of the cells. Clinically relevant inhibitors of ErbB2, lapatinib and Herceptin (traztuzumab), were used to investigate the role of ErbB2 signaling in this model. A retrospective study on a previously published breast cancer patient dataset was carried out by using Disease Specific Genomic Analysis (DSGA) to investigate the correlation of LOXL2 mRNA expression level with metastasis and survival of ErbB2-positive breast cancer patients.
resultsFluorescence staining of the acini revealed increased proliferation, decreased apoptosis, and disrupted polarity, leading to abnormal lumen formation in response to LOXL2 expression in MCF10A cells. When plated onto ECM, the LOXL2-expressing cells formed branching structures and displayed increased invasion. We noted that LOXL2 induced ErbB2 activation through reactive oxygen species (ROS) production, and ErbB2 inhibition by using Herceptin or lapatinib abrogated the effects of LOXL2 on MCF10A cells. Finally, we found LOXL2 expression to be correlated with decreased overall survival and metastasis-free survival in breast cancer patients with ErbB2-positive tumors.
conclusionsThese findings suggest that LOXL2 expression in normal epithelial cells can induce abnormal changes that resemble oncogenic transformation and cancer progression, and that these effects are driven by LOXL2-mediated activation of ErbB2. LOXL2 may also be a beneficial marker for breast cancer patients that could benefit most from anti-ErbB2 therapy.
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