Department of Gynecology, Urumqi Maternal and Child Health Hospital of Xinjiang Uygur, Urumqi, Xinjiang Uygur Autonomous Region, China.
Pathology Department, Urumqi Maternal and Child Health Hospital of Xinjiang Uygur, Urumqi, Xinjiang Uygur Autonomous Region, China.
Bioengineered. 2022 Jan;13(1):624-633. doi: 10.1080/21655979.2021.2012416.
Ovarian cancer (OC) is the main type of cancer that affects the female reproductive system and has a high morbidity and mortality rate. This study aimed to explore the regulatory effect of the chromosomal region maintenance 1 (CRM1)-survivin axis on the progression of OC. Ovarian cancer cells were transfected with pcDNA3.1-survivin and short hairpin RNA (sh)-CRM1. Cell proliferation was analyzed by cell counting kit-8 (CCK8), 5-ethynyl-2´-deoxyuridine (EdU) staining, and colony formation assays. Apoptosis was detected using flow cytometry. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting were performed to analyze the expression of RNA and protein, respectively. qRT-PCR and prognostic correlation analyses revealed that CRM1 is highly expressed in OC cells and related to survival. The results of qRT-PCR, CCK8, colony formation test, EdU staining, flow cytometry, and Western blotting showed that CRM1 silencing inhibited the proliferation and colony formation of OVCAR 3 and SKOV3 cells and promoted cell apoptosis by promoting Caspase-3 activation. Survivin was positively regulated by CRM1 and promoted the development of OC. The results of the rescue experiment showed that overexpression of survivin reversed the inhibitory effect of CRM1 knockdown on the proliferation of ovarian cancer cells and its inhibitory effect on apoptosis. Our findings confirm the role of the CRM1-survivin signal transduction axis in OC by regulating the proliferation and apoptosis of OC cells, and may thus serve as a potential therapeutic target for OC.
卵巢癌 (OC) 是影响女性生殖系统的主要癌症类型,具有较高的发病率和死亡率。本研究旨在探讨染色体维持 1 (CRM1)-survivin 轴对 OC 进展的调控作用。卵巢癌细胞转染 pcDNA3.1-survivin 和短发夹 RNA (sh)-CRM1。用细胞计数试剂盒-8 (CCK8)、5-乙炔基-2´-脱氧尿苷 (EdU) 染色和集落形成实验分析细胞增殖。用流式细胞术检测细胞凋亡。用定量实时聚合酶链反应 (qRT-PCR) 和 Western blot 分别分析 RNA 和蛋白质的表达。qRT-PCR 和预后相关性分析显示,CRM1 在 OC 细胞中高表达,并与生存相关。qRT-PCR、CCK8、集落形成试验、EdU 染色、流式细胞术和 Western blot 结果表明,CRM1 沉默通过促进 Caspase-3 激活抑制 OVCAR3 和 SKOV3 细胞的增殖和集落形成,并促进细胞凋亡。Survivin 受 CRM1 正向调节,促进 OC 的发生。挽救实验结果表明,survivin 的过表达逆转了 CRM1 敲低对卵巢癌细胞增殖的抑制作用及其对细胞凋亡的抑制作用。我们的研究结果证实了 CRM1-survivin 信号转导轴通过调节 OC 细胞的增殖和凋亡在 OC 中的作用,因此可能成为 OC 的潜在治疗靶点。