ArticleMolecular biotechnology2025
LOXL3 Silencing Hampers the Metastasis and Angiogenesis of Gastric Cancer Cells Dependent on Ferroptosis Activation.
Article in Molecular biotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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Who cites it
5 citing papers in PubMed.
- Lysyl oxidase (LOX) family proteins in extracellular matrix homeostasis: roles in disease and radiation-induced pathogenesis.Molecular biology reports · 2026Review
- FGF-23 facilitates osteosarcoma metastasis by modulating the miR-4463/LOXL2 axis expression via the ERK, p38, and JNK signaling pathway.International journal of medical sciences · 2026Article
- The "dual personality" of LOXL3: a tumor accomplice and a new hope for immunotherapy.Human cell · 2025Review
- Review
- Infection of Helicobacter pylori contributes to the progression of gastric cancer through ferroptosis.Cell death discovery · 2024Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastric cancer (GC) remains a major unmet clinical problem accountable for considerable incidence and fatality rate. Lysyl oxidase-like 3 (LOXL3) has been recognized to be overexpressed in GC. Our work was meant to disclose the significance of LOXL3 in the advancement of GC and the likely action mechanism. LOXL3 expression in GC tissues and its correlation with the outcome of GC patients were investigated through bioinformatics tools. RT-qPCR and western blotting inspected LOXL3 expression in GC cells. CCK-8 method, EDU, as well as colony formation assays assayed cell proliferation. The capacities of cells to migrate and invade were appraised by wound healing and transwell assays, severally. Tube formation assay and ELISA measured angiogenesis. TBARS, C11 BODIPY staining, and FerroOrange estimated ferroptosis. Western blotting examined the expression of proteins implicated in metastasis and ferroptosis. The up-regulation of LOXL3 expression was noticed in GC tissues and cells, which was also associated with the poor outcome of GC patients. When LOXL3 was underexpressed, the proliferation, migration, invasion, epithelial-mesenchymal transition, and angiogenesis of GC cells were all halted. In addition, LOXL3 deletion resulted in the activation of ferroptosis in GC cells, and ferrostatin-1 (Fer-1), the specific ferroptosis inhibitor, compensated the suppressive role of LOXL3 down-regulation in the proliferation, metastasis, and angiogenesis of GC cells in vitro. All in all, knockdown of LOXL3 may serve an activator of ferroptosis to obstruct the aggressive process of GC.
Indexed as
Identifiers
39192165What Socratic holds
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 Socratic graph.