ArticleCell death and differentiation2019
Derepression of LOXL4 inhibits liver cancer growth by reactivating compromised p53.
Article in Cell death and differentiation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Conserved hepatic RNA signatures across multiple cohorts reveal novel mechanistic clues for advanced fibrosis in human MASLD.Hepatology communications · 2026Pooled it
- LOXL4: a key regulatory factor at the intersection of fibrosis and tumor progression.Human cell · 2026Review
- Fusion with ARRDC1 or CD63: A Strategy to Enhance p53 Loading into Extracellular Vesicles for Tumor Suppression.Biomolecules · 2024Article
- The dual role of LOXL4 in the pathogenesis and development of human malignant tumors: a narrative review.Translational cancer research · 2024Review
- Lysyl Oxidase (LOX) Family Proteins: Key Players in Breast Cancer Occurrence and Progression.Journal of Cancer · 2024Review
- The possibilities of LOXL4 as a prognostic marker for carcinomas.Amino acids · 2023Review
- Competition between p53 and YY1 determines PHGDH expression and malignancy in bladder cancer.Cellular oncology (Dordrecht, Netherlands) · 2023Article
- Glutamate dehydrogenase1 supports HIF-1α stability to promote colorectal tumorigenesis under hypoxia.The EMBO journal · 2023Article
- Elevated Nuclear PHGDH Synergistically Functions with cMyc to Reshape the Immune Microenvironment of Liver Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Lysyl oxidase-like 3 restrains mitochondrial ferroptosis to promote liver cancer chemoresistance by stabilizing dihydroorotate dehydrogenase.Nature communications · 2023Article
- A cell transmembrane peptide chimeric M(27-39)-HTPP targeted therapy for hepatocellular carcinoma.iScience · 2023Article
- TP53 mutation-related senescence is an indicator of hepatocellular carcinoma patient outcomes from multiomics profiles.Smart medicine · 2023Article
- miR-183-5p regulates ECM and EMT to promote non-small cell lung cancer progression by targeting LOXL4.Journal of thoracic disease · 2023Article
- Lysyl Oxidase Family Proteins: Prospective Therapeutic Targets in Cancer.International journal of molecular sciences · 2022Review
- Lysyl Oxidases: Orchestrators of Cellular Behavior and ECM Remodeling and Homeostasis.International journal of molecular sciences · 2022Review
- miR-15a and miR-20b sensitize hepatocellular carcinoma cells to sorafenib through repressing CDC37L1 and consequent PPIA downregulation.Cell death discovery · 2022Article
- Genome-Wide Meta-Analysis Identifies Variants inCancers · 2022Article
- Lysyl Oxidase Family Enzymes and Their Role in Tumor Progression.International journal of molecular sciences · 2022Review
- Diagnostic Value, Prognostic Value, and Immune Infiltration ofFrontiers in oncology · 2022Article
- The Chemopreventive Role of β-Elemene in Cholangiocarcinoma by RestoringFrontiers in oncology · 2022Article
Corrections and comments
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Authors and funding
8 authors at 6 institutions in 1 country.
Funding
Abstract
TP53 is the most frequently mutated gene in human cancer, whereas tumors with wild-type TP53 develop alternative strategies to survive. Identifying new regulators of p53 reactivation would greatly contribute to the development of cancer therapies. After screening the entire genome in liver cancer cells, we identified lysyl oxidase-like 4 (LOXL4) as a novel regulator for p53 activation. We found that 5-azacytidine (5-aza-CR) induces LOXL4 upregulation, with LOXL4 subsequently binding the basic domain of p53 via its low-isoelectric point region. The interaction between LOXL4 and p53 induces the reactivation of compromised p53, resulting in cell death. Furthermore, the nude mouse xenograft model showed that the 5-aza-CR-dependent LOXL4-p53 axis reduces tumor growth. A positive correlation between LOXL4 expression and overall survival in liver cancer patients with wild-type p53 tumors was observed. In conclusion, we found that 5-aza-CR-induced LOXL4 upregulation reactivates wild-type p53 and triggers cell death, which blocks liver cancer development.
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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.