ArticleBritish journal of pharmacology2022
N-Acylethanolamine acid amidase (NAAA) is dysregulated in colorectal cancer patients and its inhibition reduces experimental cancer growth.
Article in British journal of pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Effects of Chinese herbal medicine on colorectal adenoma recurrence following polypectomy: a systematic review and meta-analysis.Frontiers in pharmacology · 2025Pooled it
- HGF knockdown suppresses ovarian cancer malignancy: insights from a transient receptor potential-related gene model.European journal of medical research · 2025Article
- Photoaffinity Labeling Reveals a Role for the Unusual Triply Acylated PhospholipidJournal of the American Chemical Society · 2025Article
- Causal relationship between the plasma lipidome and urological cancers: A two-sample Mendelian randomization study.Medicine · 2025Article
- Acetylation suppresses breast cancer progression by sustaining CLYBL stability.Journal of translational medicine · 2025Article
- Pharmacological Inhibition of N-Acylethanolamine Acid Amidase (NAAA) Mitigates Intestinal Fibrosis Through Modulation of Macrophage Activity.Journal of Crohn's & colitis · 2025Article
- Regulatory role of PPAR in colorectal cancer.Cell death discovery · 2025Review
- Comparative analysis of the short and medium-term efficacy of the Da Vinci robotWorld journal of gastrointestinal surgery · 2024Article
- Regulator of G protein signaling 16 restrains apoptosis in colorectal cancer through disrupting TRAF6-TAB2-TAK1-JNK/p38 MAPK signaling.Cell death & disease · 2024Article
- Peroxisome proliferator-activated receptors regulate the progression and treatment of gastrointestinal cancers.Frontiers in pharmacology · 2023Review
- N-Acylethanolamine acid amidase (NAAA) is dysregulated in colorectal cancer patients and its inhibition reduces experimental cancer growth.British journal of pharmacology · 2022Article
- Insights Into the Prognostic Value and Immunological Role of NAAA in Pan-Cancer.Frontiers in immunology · 2021Article
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Authors and funding
24 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeN-Acylethanolamine acid amidase (NAAA) is a lysosomal enzyme accountable for the breakdown of N-acylethanolamines (NAEs) and its pharmacological inhibition has beneficial effects in inflammatory conditions. The knowledge of NAAA in cancer is fragmentary with an unclarified mechanism, whereas its contribution to colorectal cancer (CRC) is unknown to date. EXPERIMENTAL APPROACH: CRC xenograft and azoxymethane models were used to assess the in vivo effect of NAAA inhibition. Further, the tumour secretome was evaluated by an oncogenic array, CRC cell lines were used for in vitro studies, cell cycle was analysed by cytofluorimetry, NAAA was knocked down with siRNA, human biopsies were obtained from surgically resected CRC patients, gene expression was measured by RT-PCR and NAEs were measured by LC-MS. KEY
resultsThe NAAA inhibitor AM9053 reduced CRC xenograft tumour growth and counteracted tumour development in the azoxymethane model. NAAA inhibition affected the composition of the tumour secretome inhibiting the expression of EGF family members. In CRC cells, AM9053 reduced proliferation with a mechanism mediated by PPAR-α and TRPV1. AM9053 induced cell cycle arrest in the S phase associated with cyclin A2/CDK2 down-regulation. NAAA knock-down mirrored the effects of NAAA inhibition with AM9053. NAAA expression was down-regulated in human CRC tissues, with a consequential augmentation of NAE levels and dysregulation of some of their targets. CONCLUSION AND IMPLICATIONS: Our results show novel data on the functional importance of NAAA in CRC progression and the mechanism involved. We propose that this enzyme is a valid drug target for the treatment of CRC growth and development.
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