FAT1

Official Full Name

FAT atypical cadherin 1

Organism

Homo sapiens

GeneID

2195

Background

This gene is an ortholog of the Drosophila fat gene, which encodes a tumor suppressor essential for controlling cell proliferation during Drosophila development. The gene product is a member of the cadherin superfamily, a group of integral membrane proteins characterized by the presence of cadherin-type repeats. In addition to containing 34 tandem cadherin-type repeats, the gene product has five epidermal growth factor (EGF)-like repeats and one laminin A-G domain. This gene is expressed at high levels in a number of fetal epithelia. Its product probably functions as an adhesion molecule and/or signaling receptor, and is likely to be important in developmental processes and cell communication. Transcript variants derived from alternative splicing and/or alternative promoter usage exist, but they have not been fully described. [provided by RefSeq, Jul 2008]

Synonyms

FAT; ME5; CDHF7; CDHR8; hFat1;

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Detailed Information

The FAT atypical cadherin 1 (FAT1) gene is derived from Caenorhabditis elegans C. elegans. The translation product is ω-3 polyunsaturated fatty acid dehydrogenase. The function of this enzyme is to carry out the dehydrogenation reaction with 18-20 carbon ω-6 PUFAs as a substrate to generate corresponding ω-3 PUFAs, which balances ω-in the body. The ratio of 6/ω-3 PUFAs plays an important role in the prevention and treatment of cardiovascular, cerebrovascular, tumor, schizophrenia and other diseases.

Figure 1. FAT1 is an actionable driver-oncogene in OSCC (oral squamous cell carcinoma). (Hsu, T., et al. 2019)

Anticancer Effect of FAT1 gene

A large number of studies have shown that ω-3 PUFAs in the diet are used as precursors of signal molecules during tumorigenesis, participate in the process of cell signal transduction, inhibit tumor formation at different stages, and promote tumor cell apoptosis. At present, there is a preliminary understanding of the anti-tumor effect of fat-1, but its anti-tumor mechanism is not very clear. Many mechanisms are involved in this anti-cancer effect, including inhibition of tumor cell migration, inhibition of tumor cell growth, and promotion of cell apoptosis.

The study found that compared with the control group, the fat-1 gene transgenic mice had a lower chance of developing colon cancer from colitis. Studies have confirmed that the mechanism of fat-1 transgenic mice against colon cancer caused by colitis is that ω-3 PUFAs work by inhibiting Cox-2 expression and promoting the production of PGE3 and cytokines. In addition, ω-3 PUFAs can also inhibit the formation of uterine cancer, liver tumor, and melanoma, and induce tumor cell apoptosis.

The Effect of FAT1 Gene on Cardiovascular and Cerebrovascular Diseases

Cardiovascular and cerebrovascular diseases have become the number one killer threatening human health. A large number of studies have confirmed that ω-3 PUFAs not only help prevent the occurrence of cardiovascular diseases, but also have a therapeutic effect on certain cardiovascular diseases. The fat-1 gene-transformed food can increase the content of ω-3 PUFAs in the body, which is of great significance for the prevention and treatment of cardiovascular and cerebrovascular diseases. The researchers constructed fat-1 adenovirus vector Ad. GFP-fat-1 and Ad. GFP blank vector as a reference to transfect mouse cardiomyocytes. Enzyme-linked immunoassay was used to detect the content of PGE2, the main product of ω-6 PUFAs, which was significantly lower than that of the control group.

The study found that providing ω-3 PUFAs to cardiomyocytes can resist arrhythmia. The researchers put mouse cardiomyocytes transfected with fat-1 gene and non-transgene into a high calcium (7.5mM) environment. The control group had arrhythmia. The fat-1 gene-transformed mouse cardiomyocytes maintained normal beating, indicating that the fat-1 gene was successfully integrated into the mouse cardiomyocytes, and its expression helped the cardiomyocytes to resist arrhythmia. Researchers suggest that ordinary people should consume 500mg of omega-3 PUFAs per day, while heart disease patients should consume 800-1000mg per day.

Other Functions of FAT1 Gene

Researchers add omega-3 PUFAs to the diet to optimize bone formation. Using the fat -1 mouse model to synthesize ω-3 PUFAs, it was found that when the ratio of ω-6/ω-3 PUFAs decreased, the bone mineral density (BMD) increased and the maximum load of the vertebrae was compared with that of wild Type increased. This will make the spine stronger. Studies have found that the endogenous synthesis of omega-3 PUFAs in fat-1 mice can prevent osteoporosis caused by ovariectomy. In addition, ω-3 PUFAs also play an important role in alleviating asthma attacks. The endogenous production of ω-3 PUFAs in the lungs of fat-1 mice increased, and by inducing the reduction of airway inflammation, the white blood cells accumulated in the bronchoalveolar and lung soft tissue cells decreased, thereby alleviating the onset of asthma. In addition, the reduction of the ratio of ω-6/ω-3 PUFAs can improve the animal's tolerance to glucose.

References:

Hsu, T., Huang, C., Huang, C., Huang, M., Yeh, C., Chao, T., & Bamodu, O. A. (2019). Targeting FAT1 Inhibits Carcinogenesis, Induces Oxidative Stress and Enhances Cisplatin Sensitivity through Deregulation of LRP5/WNT2/GSS Signaling Axis in Oral Squamous Cell Carcinoma. Cancers, 11(12).
Zhang, X., Liu, J., Liang, X., Chen, J., Hong, J., Li, L., & Cai, X. (2016). History and progression of Fat cadherins in health and disease. OncoTargets and Therapy, 7337-7343.
Helmbacher, F. (2018). Tissue-specific activities of the Fat1 cadherin cooperate to control neuromuscular morphogenesis. PLOS Biology, 16(5).

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