Department of Gynaecology and Obstetrics, Linyi City Central Hospital, Linyi, China.
Eur Rev Med Pharmacol Sci. 2018 Feb;22(3):616-622. doi: 10.26355/eurrev_201802_14284.
To investigate the expression of long non-coding RNA SNHG16 in ovarian cancer and to further investigate its role in the development of ovarian cancer as well as its potential regulatory mechanism.
Quantitative Real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of SNHG16 in 103 ovarian cancer tissues and normal tissues; the relationship between the expression of SNHG16 and the pathological parameters of ovarian cancer and the prognosis of patients was also analyzed. qRT-PCR was used to further verify the expression of SNHG16 in the ovarian cancer cells. After establishment of SNHG16 knockdown expression model in ovarian cancer cells SKOV-3 and HO8910 using small interfering RNA, the effect of SNHG16 on biological function of ovarian cancer cells was analyzed via cell counting kit-8 (CCK8), transwell invasion and migration assay. Finally, its potential mechanism was analyzed by Western Blot.
qRT-PCR results showed that the expression of SNHG16 in ovarian cancer was significantly higher than that in normal tissues, and the difference was statistically significant. Compared with patients with lower expression of SNHG16, patients with higher expression of SNHG16 had higher tumor stage, high rate of distant metastasis and low overall survival rate. Compared with the negative control si-NC group, the cell proliferation, invasion and migration ability in SNHG16 knockdown group (si-SNHG16) significantly decreased. Western Blot showed that after knockdown of SNHG16, expressions of P-AKT and MMP9 decreased significantly, while there was no significant change in the total AKT level.
SNHG16 was highly expressed in ovarian cancer, and was correlated with staging, distant metastasis and poor prognosis of ovarian cancer. SNHG16 may activate phosphorylation of AKT and upregulate the expression of MMP9 to promote cell proliferation, invasion and migration of ovarian cancer.
研究长链非编码 RNA SNHG16 在卵巢癌中的表达，进一步探讨其在卵巢癌发展中的作用及其潜在的调控机制。
采用实时定量聚合酶链反应（qRT-PCR）检测 103 例卵巢癌组织和正常组织中 SNHG16 的表达，分析 SNHG16 的表达与卵巢癌病理参数及患者预后的关系。qRT-PCR 进一步验证卵巢癌细胞中 SNHG16 的表达。采用小干扰 RNA 建立卵巢癌细胞 SKOV-3 和 HO8910 中 SNHG16 敲低表达模型，通过细胞计数试剂盒-8（CCK8）、Transwell 侵袭和迁移实验分析 SNHG16 对卵巢癌细胞生物学功能的影响。最后，通过 Western blot 分析其潜在机制。
qRT-PCR 结果显示，卵巢癌中 SNHG16 的表达明显高于正常组织，差异有统计学意义。与 SNHG16 低表达患者相比，SNHG16 高表达患者的肿瘤分期较高，远处转移率较高，总生存率较低。与阴性对照 si-NC 组相比，SNHG16 敲低组（si-SNHG16）的细胞增殖、侵袭和迁移能力明显降低。Western blot 显示，敲低 SNHG16 后，P-AKT 和 MMP9 的表达明显下降，而总 AKT 水平没有明显变化。
SNHG16 在卵巢癌中高表达，与卵巢癌的分期、远处转移和不良预后相关。SNHG16 可能通过激活 AKT 的磷酸化，上调 MMP9 的表达，促进卵巢癌细胞的增殖、侵袭和迁移。
