Department of Gynecology, Chengyang People's Hospital, Qingdao, Shandong, China (mainland).
Department of Geriatrics, Chengyang People's Hospital, Qingdao, Shandong, China (mainland).
Med Sci Monit. 2019 Jan 30;25:856-865. doi: 10.12659/MSM.913058.
BACKGROUND E74-like factor 5 (ELF5) plays a key role in the processes of cell differentiation, apoptosis, and occurrence of tumors. However, the effect of ELF5 on metastasis and invasion in human ovarian cancer remains poorly understood. MATERIAL AND METHODS Quantitative real-time polymerase chain reaction (qPCR) was performed to measure the expression of ELF5. The viability of cells was detected by cell counting kit (CCK-8). Cell apoptosis was tested by flow cytometry. Matrigel plug angiogenesis assay was employed to determine angiogenesis rate. The protein expression levels of vascular endothelial growth factor (VEGF), cleaved caspase-3, B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), E-cadherin, N-cadherin, Snail, phosphoinositide 3 kinase (PI3K), phosphorylated (p)-PI3K, tyrosine kinase B (AKT), and phosphorylated (p)-AKT were determined by Western blot. Wound-healing assay and Transwell were used to determine invasion and migration. RESULTS We found that expression of ELF5 was obviously decreased in ovarian cancer cell lines. The cells viability, invasion and metastasis were inhibited by overexpression ELF5. ELF5 suppressed angiogenesis rate and the expression of VEGF. Changes of the expressions of Bcl-2, cleaved caspase-3 and Bax showed that anti-apoptosis ability was improved by ELF5. ELF5 also repressed N-cadherin and Snail and increased E-cadherin. The expressions of p-PI3K and p-AKT were decreased by ELF5. Further study showed that IGF-I reversed the inhibitory effect of ELF5 on growth and metastasis of SKOV3 cells. CONCLUSIONS Overexpression of ELF5 promoted the apoptosis and reduced the migration and invasion of ovarian cancer cells; therefore, it could provide a new approach to gene treatment of ovarian carcinoma.
E74 样因子 5（ELF5）在细胞分化、细胞凋亡和肿瘤发生过程中发挥关键作用。然而，ELF5 对人卵巢癌转移和侵袭的影响仍知之甚少。
采用实时定量聚合酶链反应（qPCR）检测 ELF5 的表达。通过细胞计数试剂盒（CCK-8）检测细胞活力。采用流式细胞术检测细胞凋亡。采用 Matrigel 塞血管生成试验检测血管生成率。采用 Western blot 检测血管内皮生长因子（VEGF）、裂解的半胱氨酸天冬氨酸蛋白酶-3（cleaved caspase-3）、B 细胞淋巴瘤 2（Bcl-2）、Bcl-2 相关 X 蛋白（Bax）、上皮钙黏蛋白（E-cadherin）、神经钙黏蛋白（N-cadherin）、Snail、磷酸肌醇 3 激酶（PI3K）、磷酸化（p）-PI3K、酪氨酸激酶 B（AKT）和磷酸化（p）-AKT 的蛋白表达水平。通过划痕愈合试验和 Transwell 检测侵袭和迁移。
我们发现 ELF5 在卵巢癌细胞系中的表达明显降低。过表达 ELF5 可抑制细胞活力、侵袭和转移。ELF5 抑制血管生成率和 VEGF 的表达。Bcl-2、cleaved caspase-3 和 Bax 的表达变化表明 ELF5 可改善抗凋亡能力。ELF5 还抑制 N-cadherin 和 Snail 并增加 E-cadherin。ELF5 可降低 p-PI3K 和 p-AKT 的表达。进一步研究表明，IGF-I 逆转了 ELF5 对 SKOV3 细胞生长和转移的抑制作用。
过表达 ELF5 可促进卵巢癌细胞凋亡，并降低其迁移和侵袭能力；因此，它可为卵巢癌的基因治疗提供新途径。
