Department of Oncology, ZhuJiang Hospital of Southern Medical University, Guangzhou, China.
Department of Oncology, Yan'an People's Hospital, Yan'an, China.
Kaohsiung J Med Sci. 2017 Sep;33(9):427-432. doi: 10.1016/j.kjms.2017.05.015. Epub 2017 Jul 10.
Radioresistance remains a major problem in nasopharyngeal carcinoma (NPC) treatment. However, the underlying molecular mechanisms of NPC radioresistance remain poorly understood. The present study aimed to investigate the potential role and mechanism of miR-206 in NPC radioresistance. We observed that miR-206 was down-regulated in radioresistant NPC cells. Furthermore, restoration of miR-206 in CNE2-IR cells suppressed enhanced radiosensitivity of NPC cells. In contrast, inhibition of miR-206 in CNE2 cells reduced the radiosensitivity. We also found that miR-206 directly targeted IGF1 and inhibited the PI3K/AKT pathway. Our data demonstrate that miR-206 sensitizes NPC cell to irradiation by targeting IGF1, highlighting the therapeutic potential of miR-206 in NPC radiosensitization.
放射抵抗仍然是鼻咽癌(NPC)治疗中的一个主要问题。然而,NPC 放射抵抗的潜在分子机制仍了解甚少。本研究旨在探讨 miR-206 在 NPC 放射抵抗中的潜在作用和机制。我们观察到 miR-206 在放射抵抗的 NPC 细胞中下调。此外,在 CNE2-IR 细胞中恢复 miR-206 抑制了 NPC 细胞放射敏感性的增强。相反,在 CNE2 细胞中抑制 miR-206 降低了放射敏感性。我们还发现 miR-206 可以直接靶向 IGF1 并抑制 PI3K/AKT 通路。我们的数据表明,miR-206 通过靶向 IGF1 使 NPC 细胞对辐射敏感,突出了 miR-206 在 NPC 放射增敏中的治疗潜力。