DPCPX induces Bim-dependent apoptosis in nasopharyngeal carcinoma cells

ADORA1 promotes tumor growth and development in multiple cancers. DPCPX (a selective adenosine Al receptor antagonist), a specific ADORA1 antagonist, has shown antitumor effects in many cancer types. Nevertheless, the function of DPCPX in nasopharyngeal carcinoma (NPC) still remains to be unraveled. In this study, we investigated the functional role of DPCPX on NPC cells. We found that DPCPX promotes NPC cells growth inhibition. DPCPX induced Bim-dependent apoptosis in NPC cells irrespective of p53 status via the FoxO3a pathway following PI3K/AKT inhibition. Furthermore, DPCPX enhanced the antitumor effect of cisplatin, 5-FU and Paclitaxel in NPC. Xenograft experiment revealed that deficiency of Bim in vivo stalls apoptosis and antitumor activity of DPCPX. In conclusion, the PI3K/AKT/ FoxO3a/Bim axis plays a critical role in the anticancer effects of DPCPX in NPC.

Automated summary

This study reveals the inhibitory effects of DPCPX on nasopharyngeal carcinoma (NPC). By inhibiting the PI3K/AKT pathway, DPCPX induces Bim-dependent apoptosis and suppresses NPC cell growth. Additionally, DPCPX enhances the antitumor effects of chemotherapy drugs such as cisplatin, 5-FU, and Paclitaxel.