ArticleCancer medicine2015
Effects of human arylamine N-acetyltransferase I knockdown in triple-negative breast cancer cell lines.
Article in Cancer medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 47 citations in OpenAlex.
- Arylamine N-Acetyltransferase 1 Knockout in Immortalized Human Bronchial Cells Results in a Reduction of Cellular Growth.Gene reports · 2025Article
- Investigating the mechanisms by which low NAT1 expression in tumor cells contributes to chemo-resistance in colorectal cancer.Clinical epigenetics · 2025Article
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- Arylamine N-acetyltransferase 1 deficiency inhibits drug-induced cell death in breast cancer cells: switch from cytochrome C-dependent apoptosis to necroptosis.Breast cancer research and treatment · 2022Article
- Deletion of arylamine N-acetyltransferase 1 in MDA-MB-231 human breast cancer cells reduces primary and secondary tumor growth in vivo with no significant effects on metastasis.Molecular carcinogenesis · 2022Article
- Identification and characterization of potent, selective, and efficacious inhibitors of human arylamine N-acetyltransferase 1.Archives of toxicology · 2022Article
- Proteomic analysis of arylamineToxicology reports · 2022Article
- The Role of Noncoding RNAs in the Regulation of Anoikis and Anchorage-Independent Growth in Cancer.International journal of molecular sciences · 2021Review
- Human ArylamineFrontiers in pharmacology · 2021Article
- B4GALNT2 Gene Promotes Proliferation, and Invasiveness and Migration Abilities of Model Triple Negative Breast Cancer (TNBC) Cells by Interacting With HLA-B Protein.Frontiers in oncology · 2021Article
- Effect arylamine N-acetyltransferase 1 on morphology, adhesion, migration, and invasion of MDA-MB-231 cells: role of matrix metalloproteinases and integrin αV.Cell adhesion & migration · 2020Article
- CRISPR/Cas9 knockout of human arylamine N-acetyltransferase 1 in MDA-MB-231 breast cancer cells suggests a role in cellular metabolism.Scientific reports · 2020Article
- MicroRNA-6744-5p promotes anoikis in breast cancer and directly targets NAT1 enzyme.Cancer biology & medicine · 2020Article
- Prognostic and Clinicopathological Significance of X-Box-Binding Protein 1 and N-Acetyltransferase 1 in Gallbladder Cancer.Frontiers in oncology · 2020Article
- NAT1 promotes osteolytic metastasis in luminal breast cancer by regulating the bone metastatic niche via NF-κB/IL-1B signaling pathway.American journal of cancer research · 2020Article
- Population variability of rhesus macaque (Macaca mulatta) NAT1 gene for arylamine N-acetyltransferase 1: Functional effects and comparison with human.Scientific reports · 2019Article
- Epithelial-to-mesenchymal transition status of primary breast carcinomas and its correlation with metastatic behavior.Breast cancer research and treatment · 2019Article
- Article
- Knockout of human arylamine N-acetyltransferase 1 (NAT1) in MDA-MB-231 breast cancer cells leads to increased reserve capacity, maximum mitochondrial capacity, and glycolytic reserve capacity.Molecular carcinogenesis · 2018Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Expression of human arylamine N-acetyltransferase I (NAT1) has been associated with various cancer subtypes and inhibition of this enzyme with small molecule inhibitors or siRNA affects cell growth and survival. Here, we have investigated the role of NAT1 in the invasiveness of breast cancer cells both in vitro and in vivo. We knocked down NAT1 using a lentivirus-based shRNA approach and observed marked changes in cell morphology in the triple-negative breast cancer cell lines MDA-MB-231, MDA-MB-436, and BT-549. Most notable was a reduction in the number and size of the filopodia protrusions on the surface of the cells. The loss of filopodia could be rescued by the reintroduction of NAT1 into the knockdown cells. NAT1 expression was localized to the lamellipodia and extended into the filopodia protrusions. In vitro invasion through Geltrex was significantly inhibited in both the MDA cell lines but not in the BT-549 cells. The expression of Snail increased when NAT1 was knocked down, while other genes associated with mesenchymal to epithelial transition (vimentin, cytokeratin-18, and Twist) did not show any changes. By contrast, both N-cadherin and β-catenin were significantly reduced. When MDA-MB-231 cells expressing shRNA were injected in vivo into BALB/c nu/nu nude mice, a significant reduction in the number of colonies that formed in the lungs was observed. Taken together, the results show that NAT1 can alter the invasion and metastatic properties of some triple-negative breast cancer cells but not all. The study suggests that NAT1 may be a novel therapeutic target in a subset of breast cancers.
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