Abstract
Complement 5a (C5a) is able to induce the proliferation of human nasopharyngeal carcinoma (NPC) cells. Therefore, an effective method or drug that can specifically inhibit C5a-induced proliferation of human NPC cells needs to be developed. Reportedly, Apigenin has antiproliferative effects on a variety of cancer cells. However, the effect of Apigenin on NPC cell proliferation and its underlying mechanism are still unclear. Herein, the present study aimed to evaluate the effect of Apigenin on C5a-induced proliferation of human NPC cells and its possible mechanism through down-regulation of C5aR. We revealed that Apigenin in vitro could not only inhibit proliferation of NPC cells and but also reduce the expression of C5aR and P300/CBP-associated factor (PCAF) as well as the activation of signal transducer and activator of transcription 3 (STAT3) in NPC cells. Furthermore, Apigenin reduced the proliferation of human NPC cells triggered by C5a through negative regulation of C5aR/PCAF/STAT3 axis. These might provide a new insight into the function of Apigenin in cancer treatment, and also provide a potential strategy for treating human NPC through inhibition of C5aR expression on cancer cells.
Highlights
Nasopharyngeal carcinoma (NPC) is a common tumor in the head and neck arising from the epithelium of the nasopharynx [1,2]
The result showed that Apigenin treatment could not significantly inhibit the proliferation of C666-1 nasopharyngeal carcinoma cells (C666-1) cells induced by complement 5a (C5a) (Figure 1A)
These data suggest that Apigenin might inhibit NPC cell proliferation exposed to C5a possibly at the C5a-C5aR level
Summary
Nasopharyngeal carcinoma (NPC) is a common tumor in the head and neck arising from the epithelium of the nasopharynx [1,2]. It is one of the most common malignancies in Southern China and Southeast Asia with an incidence rate of 20–30 per 100000, accounting for approximately 40% of the world’s new cases [3,4,5]. Cai et al [13] reported that C5a could promote the proliferation of human NPC cells through p300/CBP-associated factor (PCAF)-mediated acetylation of signal transducer and activator of transcription 3 (STAT3). An effective method or drug that can inhibit C5a-induced proliferation of human NPC cells needs to be developed
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