ArticleCell death and differentiation2018
Lysyl oxidase-like 3 is required for melanoma cell survival by maintaining genomic stability.
Article in Cell death and differentiation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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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.
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.
Who cites it
28 citing papers in PubMed, 58 citations in OpenAlex.
- In vitro functional analysis of lysyl oxidase family members in highly metastatic pancreatic cancer cells derived from a syngeneic orthotopic model.BMC cancer · 2026Article
- PAIR: Reconstructing Single-Cell Open-Chromatin Landscapes for Transcription Factor Regulome Mapping.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- The "dual personality" of LOXL3: a tumor accomplice and a new hope for immunotherapy.Human cell · 2025Review
- Review
- Pulmonary lysyl oxidase expression and its role in seeding Lewis lung carcinoma cells.Clinical & experimental metastasis · 2024Article
- Low-dose arsenic trioxide inhibits pancreatic stellate cell activation via LOXL3 expression to enhance immunotherapy in pancreatic cancer.British journal of cancer · 2024Article
- Expression ofCells · 2024Article
- LOXL2 in Cancer: A Two-Decade Perspective.International journal of molecular sciences · 2023Review
- LncRNA CFAR promotes cardiac fibrosis via the miR-449a-5p/LOXL3/mTOR axis.Science China. Life sciences · 2023Article
- N6-methyladenosine reader YTHDF3 regulates melanoma metastasis via its 'executor'LOXL3.Clinical and translational medicine · 2022Article
- Lysyl Oxidase Family Proteins: Prospective Therapeutic Targets in Cancer.International journal of molecular sciences · 2022Review
- Article
- Correlation of Matrisome-Associatted Gene Expressions with LOX Family Members in Astrocytomas Stratified by IDH Mutation Status.International journal of molecular sciences · 2022Article
- Lysyl Oxidase Family Enzymes and Their Role in Tumor Progression.International journal of molecular sciences · 2022Review
- Loxl3 Promotes Melanoma Progression and Dissemination Influencing Cell Plasticity and Survival.Cancers · 2022Article
- CaFrontiers in cardiovascular medicine · 2022Article
- Apoptosis Activation and Autophagy Inhibition of Chondrocytes by Leptin by the Upregulation of LOXL3 in Osteoarthritis Pathogenesis.Journal of healthcare engineering · 2022Article
- LOXL3 Silencing Affected Cell Adhesion and Invasion in U87MG Glioma Cells.International journal of molecular sciences · 2021Article
- Targeting Genome Stability in Melanoma-A New Approach to an Old Field.International journal of molecular sciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Lysyl oxidase-like 3 (LOXL3) is a member of the lysyl oxidase family comprising multifunctional enzymes with depicted roles in extracellular matrix maturation, tumorigenesis, and metastasis. In silico expression analyses followed by experimental validation in a comprehensive cohort of human cell lines revealed a significant upregulation of LOXL3 in human melanoma. We show that LOXL3 silencing impairs cell proliferation and triggers apoptosis in various melanoma cell lines. Further supporting a pro-oncogenic role in melanoma, LOXL3 favors tumor growth in vivo and cooperates with oncogenic BRAF in melanocyte transformation. Upon LOXL3 depletion, melanoma cells display a faulty DNA damage response (DDR), characterized by ATM checkpoint activation and inefficient ATR activation leading to the accumulation of double-strand breaks (DSBs) and aberrant mitosis. Consistent with these findings, LOXL3 binds to proteins involved in the maintenance of genome integrity, in particular BRCA2 and MSH2, whose levels dramatically decrease upon LOXL3 depletion. Moreover, LOXL3 is required for efficient DSB repair in melanoma cells. Our results reveal an unexpected role for LOXL3 in the control of genome stability and melanoma progression, exposing its potential as a novel therapeutic target in malignant melanoma, a very aggressive condition yet in need for more effective treatment options.
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Registered trials
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.