Abstract
Osajin is a prenylated isoflavone showing antitumor activity in different tumor cell lines. The underlying mechanism of osajin-induced cancer cell death is not clearly understood. In the present study, the mechanisms of osajin-induced cell death of human nasopharyngeal carcinoma (NPC) cells were explored. Osajin was found to significantly induce apoptosis of NPC cells in a dose- and time-dependent manner. Multiple molecular effects were observed during osajin treatment including a significant loss of mitochondrial transmembrane potential, release of cytochrome c into the cytosol, enhanced expression of Fas ligand (FasL), suppression of glucose-regulated protein 78 kDa (GRP78), and activation of caspases-9, -8, -4 and -3. In addition, up-regulation of proapoptotic Bax protein and down-regulation of antiapoptotic Bcl-2 protein were also observed. Taken together, osajin induces apoptosis in human NPC cells through multiple apoptotic pathways, including the extrinsic death receptor pathway, and intrinsic pathways relying on mitochondria and endoplasmic reticulum stress. Thus, osajin could be developed as a new effective and chemopreventive compound for human NPC.
Highlights
The flavonoids are a heterogeneous group of phenolic compounds showing diverse biological effects such as antioxidant, antiviral, anticancer, anti-inflammatory, and antiallergic activities [1,2]
Osajin reduces the viability of human nasopharyngeal carcinoma (NPC) cells The effects of osajin on the viability of human NPC cells were first studied
Three different types of NPC cell lines were treated with increasing concentrations of osajin for 24 h, and were followed by the MTT assay
Summary
The flavonoids are a heterogeneous group of phenolic compounds showing diverse biological effects such as antioxidant, antiviral, anticancer, anti-inflammatory, and antiallergic activities [1,2]. Flavonoids are frequently used in oncology to reduce the side effects of cytostatics and enhance the therapeutic effects [3,4]. Osajin is a flavonoid compound isolated from the fruit of Maclura pomifera, a tree belonging to the Moraceae or mulberry family, and is commonly referred to as ‘‘osajin orange, hedge apple, bow wood, and horse apple’’ [5,6]. Osajin exhibits growth inhibitory activity on six human cancer cell lines, including kidney, lung, prostate, breast, melanoma and colon cancer cells [8]. Despite the increasing therapeutic interest in osajin, the mechanisms of action of osajin on nasopharyngeal carcinoma (NPC) cells remain unaddressed
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