Third Department of Neurosurgery, Affiliated Hospital of Hebei University of Engineering, Handan, Hebei, People's Republic of China.
Technol Cancer Res Treat. 2020 Jan-Dec;19:1533033820977536. doi: 10.1177/1533033820977536.
To explore the role and mechanism of CERS1 in hypophysoma and investigate whether CERS1 overexpression can change the autophagy process of hypophysoma, and then to explore whether CERS1's effect was regulated by the PI3K/AKT signaling pathway. Western blot and RT-PCR were used to analyze the expression or mRNA level of CERS1 at different tissues or cell lines. Afterwards, the occurrence and development of hypophysoma in vivo and in vitro, respectively, was observed by using CERS1 overexpression by lentivirus. Finally, MK-2206 and LY294002 were applied to discuss whether the role of CERS1 was regulated by the PI3K/AKT signaling pathway. Results show that the CERS1 expression and mRNA level in tumor or AtT-20 cells were decreased. CERS1 over-expressed by lentivirus could inhibit hypophysoma development in vivo and in vitro by reducing tumor volume and weight, weakening tumor proliferation and invasion, and enhancing apoptosis. In addition, shCERS1 could reverse the process. The above results indicate that CERS1 is possibly able to enhance autophagy in hypophysoma through the PI3K/AKT signaling pathway.
探讨 CERS1 在垂体瘤中的作用和机制，研究 CERS1 过表达是否能改变垂体瘤的自噬过程，进一步探讨 CERS1 的作用是否受 PI3K/AKT 信号通路的调控。方法：通过 Western blot 和 RT-PCR 分析不同组织或细胞系中 CERS1 的表达或 mRNA 水平。然后，通过慢病毒过表达 CERS1 分别观察体内和体外垂体瘤的发生和发展。最后，应用 MK-2206 和 LY294002 探讨 CERS1 的作用是否受 PI3K/AKT 信号通路调控。结果：结果显示，肿瘤或 AtT-20 细胞中的 CERS1 表达和 mRNA 水平降低。通过慢病毒过表达 CERS1 可减少肿瘤体积和重量，减弱肿瘤增殖和侵袭，增强凋亡，从而抑制体内和体外垂体瘤的发展。此外，shCERS1 可逆转这一过程。上述结果表明，CERS1 可能通过 PI3K/AKT 信号通路增强垂体瘤中的自噬。
