The Akt adenovirus is a recombinant viral vector used to deliver the Akt gene, a key regulator of cell survival, proliferation, and metabolism. The Akt gene, also known as protein kinase B (PKB), plays a key role in the PI3K-Akt signaling pathway, which is involved in processes such as glucose uptake, apoptosis inhibition, and cell growth. This adenoviral vector system was chosen for its high transduction efficiency, ability to infect both dividing and non-dividing cells, and ability to achieve high-level transgene expression. Akt adenoviruses are typically replication-defective, ensuring safety for both experimental and therapeutic applications while effectively delivering the Akt gene to target cells. This tool is widely used in molecular biology and biomedical research to investigate the functional role of Akt in various cellular contexts, including cancer, metabolic disorders, and cardiovascular disease.
Akt adenovirus has a wide range of applications in both basic and preclinical research. In cancer research, overactivation of the Akt pathway is common in tumors, leading to its use in exploring its oncogenic potential. By overexpressing Akt in cell lines or animal models, researchers can mimic pathological conditions and explore the mechanisms of tumor progression, drug resistance, and metastasis. Furthermore, Akt adenovirus is used in regenerative medicine to investigate its role in promoting cell survival and tissue repair, particularly in models of cardiac and neuronal injury. In metabolic research, this tool has helped elucidate how Akt regulates insulin signaling and blood glucose homeostasis, providing new insights into the treatment of diabetes and obesity. Beyond research, Akt adenovirus also has potential for gene therapy, where controlling Akt expression may help treat diseases characterized by excessive cell death or impaired proliferation.
Ferulic acid, a phenolic acid widely found in corn, wheat, and flax, has potent antitumor effects in various cancer cell lines. However, the antitumor effects of ferulic acid on osteosarcoma remain unclear. Here, the researchers examined the effects of ferulic acid on osteosarcoma cells and explored its potential mechanisms. MTT assay and Annexin V-FITC apoptosis assay showed that ferulic acid dose-dependently inhibited the proliferation of 143B and MG63 osteosarcoma cells and induced apoptosis. In addition, flow cytometry assay and Western blotting confirmed that ferulic acid induced G0/G1 phase arrest and downregulated the expression of cell cycle-related proteins CDK 2, CDK 4, and CDK 6. In addition, ferulic acid upregulated Bax, downregulated Bcl-2, and subsequently enhanced caspase-3 activity. More importantly, ferulic acid dose-dependently inhibited PI3K/Akt activation. The antiproliferative and pro-apoptotic effects of ferulic acid were reversed using adenovirus expressing active Akt. These results suggest that ferulic acid may inhibit proliferation and induce apoptosis by inhibiting the PI3K/Akt pathway in osteosarcoma cells. Ferulic acid is a new therapeutic drug for osteosarcoma.
To determine whether the PI3K/Akt pathway is involved in the antitumor effect of ferulic acid, the protein level of activated Akt (p-Akt) in human osteosarcoma cells was detected by IF and WB. As shown in Figures 1A and 1B, p-Akt in MG63 cells was significantly reduced after ferulic acid treatment in a dose-dependent manner. To further determine the effect of inhibition of the PI3K/Akt pathway on the antitumor effect of ferulic acid, cells were treated with LY294002, a specific inhibitor of PI3K. As shown in Figures 1C and 1D, LY294002 also had an antitumor effect, which was similar to ferulic acid. In addition, overexpression of active Akt in the adenovirus (Ad-AKT) system reversed the antitumor effect of ferulic acid, eliminating the inhibitory effect on cell proliferation and promoting apoptosis (Figures 1C and 1D).
Figure 1. Effect of ferulic acid on PI3K/AKT signal activation in osteosarcoma cells. (Wang T, et al., 2016)
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