Fatty acid binding protein 4 (FABP4), also known as adipocyte FABP (A-FABP), is a key regulator of lipid metabolism and inflammatory responses. The gene encodes a small cytoplasmic protein that is highly expressed in adipocytes and macrophages and facilitates the transport and storage of fatty acids within the cell. FABP4 plays a key role in metabolic disorders such as obesity, insulin resistance, and atherosclerosis by regulating lipolysis, glucose homeostasis, and cytokine production. Studies have also linked FABP4 to cancer progression, as it promotes tumor cell proliferation and metastasis through metabolic reprogramming. Therefore, FABP4 is a promising therapeutic target for metabolic and inflammatory diseases.
Human FABP4 Adenoviral Particles are a replication-defective viral vector designed to deliver the FABP4 gene to target cells for overexpression studies. Adenoviral systems are favored for their high transduction efficiency, broad tropism, and ability to infect both dividing and non-dividing cells. These particles are carefully designed to ensure safety, with the E1/E3 regions deleted to prevent replication while maintaining stable transgene expression. Researchers have used FABP4 adenoviral particles to study the role of this gene in metabolic pathways, inflammation, and cancer biology, providing key insights into disease mechanisms.
Colon cancer metastasis carries a poor prognosis, but its mechanisms, especially those related to adipocytes, remain unclear. Fatty acid binding proteins (FABPs) are a class of homologous small cytoplasmic proteins that bind and transport hydrophobic fatty acids. FABP4, a member of this family, is highly expressed in adipose tissue and macrophages. Here, researchers observed higher lipid accumulation and stronger FABP4 transcription in colon cancer tissues. After incubation with adipose tissue extracts and overexpression of FABP4, colon cancer cells showed enhanced lipid accumulation. In functional experiments, co-culture with adipose tissue extracts significantly enhanced the invasion and migration of colon cancer cells, as well as energy and lipid metabolism, all of which were reversed by FABP4 inhibitors. In addition, the metastasis of colon cancer cells overexpressing FABP4 was also significantly enhanced in both in vivo and in vitro experiments. In terms of mechanism, bioinformatics analysis showed that FABP4 was enriched in 11 pathways related to metabolic processes in overexpressing cells. Finally, FABP4 overexpression promotes EMT progression in colon cancer, as evidenced by upregulation of Snail, MMP-2, and MMP-9, downregulation of E-cadherin, and increased expression of p-Akt. These studies indicate that FABP4 overexpression can increase fatty acid transport, enhance energy and lipid metabolism, activate the AKT pathway and EMT, and promote migration and invasion of colon cancer cells.
To further explore the mechanism of action of FABP4 in colon cancer metastasis, FABP4 recombinant adenovirus was used to confirm that FABP4 was involved in the progression of colon cancer. In HCT-8 cells, the number of transmembrane cells in the FABP4 overexpression group was 1.70±0.03 times that of the control group (Figure 1d). The width of the "scratch" in the FABP4 overexpression group after 24 hours of scratching was 76% of that in the control group (Figure 1e). However, there was no change in the proliferation of cancer cells (Figure 1f). Similar results were observed in HCT-116 cells. Overall, these results indicate that FABP4 enhances the invasion and migration of colon cancer cells but does not change their proliferation.
Figure 1. FABP4 enhanced the invasion and migration, but did not change the proliferation of colon cancer cells. (Tian W, et al., 2020)
Customer Reviews
Cost-Effective Solution
Compared to other vendors, Creative Biogene offers high-quality adenoviral particles at a competitive price. Great value!
Write a Review