Yanwei Li, Yinli Yang, Pan Zhanyu
Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, China.
Key Laboratory of Cancer Prevention and Therapy, Tianjin, China.
Evid Based Complement Alternat Med. 2018 Feb 13;2018:5291517. doi: 10.1155/2018/5291517. eCollection 2018.
Antiangiogenic therapy is vital in nasopharyngeal carcinoma (NPC) treatment. NPC01 has already been successfully used in treating patients with NPC in clinical practice and exerted an excellent antiangiogenetic effect. However, the potential molecular mechanism underlying the antitumor effect of NPC01 has not been well explored. The present study demonstrated that NPC01 could significantly inhibit cell proliferation and induce cell apoptosis in a dose-dependent manner in human NPC cell lines. Furthermore, NPC01 exerted antiproliferative and antiangiogenic effects in NPC xenograft mice. Moreover, the study showed that NPC01 could significantly decrease the expression of angiogenesis-associated factors including hypoxia-inducible factor-1 and vascular endothelial growth factor. Additionally, the decreased expression of these angiogenesis-associated factors could be due to the inhibition of the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway (PI3K/Akt/mTOR). In conclusion, the results proposed that NPC01 could exert its antitumor effect by suppressing the PI3K/Akt/mTOR signaling pathway. Further studies are warranted to elucidate the molecular mechanism.
抗血管生成疗法在鼻咽癌（NPC）治疗中至关重要。NPC01已在临床实践中成功用于治疗鼻咽癌患者，并发挥了出色的抗血管生成作用。然而，NPC01抗肿瘤作用的潜在分子机制尚未得到充分探索。本研究表明，NPC01能以剂量依赖的方式显著抑制人鼻咽癌细胞系的细胞增殖并诱导细胞凋亡。此外，NPC01在鼻咽癌异种移植小鼠中发挥了抗增殖和抗血管生成作用。而且，该研究表明NPC01能显著降低包括缺氧诱导因子-1和血管内皮生长因子在内的血管生成相关因子的表达。此外，这些血管生成相关因子表达的降低可能是由于磷酸肌醇3激酶（PI3K）/蛋白激酶B（Akt）/雷帕霉素哺乳动物靶蛋白（mTOR）信号通路（PI3K/Akt/mTOR）受到抑制。总之，结果表明NPC01可通过抑制PI3K/Akt/mTOR信号通路发挥其抗肿瘤作用。有必要进行进一步研究以阐明其分子机制。
