Yao Zhilan, Shu Liuping, Yi Yi, Qiao Lifu
Department of Gynecology, Wujin Hospital Affiliated with Jiangsu University, Changzhou, Jiangsu Province, 213100, People's Republic of China.
Department of Gynecology, The Wujin Clinical College of Xuzhou Medical University, Changzhou, Jiangsu Province, 213100, People's Republic of China.
Cancer Manag Res. 2021 Jun 30;13:5211-5222. doi: 10.2147/CMAR.S302201. eCollection 2021.
Cervical cancer (CC) is the fourth most common cancer among women worldwide. We aimed to explore the role of hsa_circ_000543 played in CC.
The hsa_circ_000543 expressions in CC tissues and cells were measured by qRT-PCR. The correlation of hsa_circ_000543 expression and the clinical features of CC patients were analyzed by SPSS 20.0. The up- or down-regulated plasmids of hsa_circ_000543 were respectively transfected into CC cells. Cell proliferation, apoptosis and colony formation were detected through CCK-8 assay, flow cytometry and cell colony formation assay, respectively. The cell migration and invasion were evaluated by Transwell assay. The underlying molecular mechanism of hsa_circ_000543 was studied by bioinformatic prediction tools and luciferase reporter assay. Rescue experiments were performed to validate the regulation mechanism of hsa_circ_000543/miR-567/ZNF268 axis in CC.
Hsa_circ_000543 was over-expressed in CC tissues and cells. The high expression of hsa_circ_000543 indicated poor prognosis of CC patients. Hsa_circ_000543 promoted cell proliferation, colony formation, migration and invasion, as well as inhibited cell apoptosis in CC cells. Hsa_circ_000543 directly targeted miR-567/ZNF268 in CC cell lines. In CC tumor tissues and cells, the hsa_circ_000543 expression was negatively correlated with miR-567 expression and showed a positive correlation with ZNF268 expression. The rescue experiments revealed that hsa_circ_000543 mediated cell proliferation, apoptosis, colony formation, migration and invasion of CC cells via regulating miR-567/ZNF268 axis.
Hsa_circ_000543 regulated CC cell activities through binding miR-567 and therefore enhancing ZNF268 expression.
宫颈癌（CC）是全球女性中第四大常见癌症。我们旨在探讨hsa_circ_000543在宫颈癌中所起的作用。
采用qRT-PCR检测宫颈癌组织和细胞中hsa_circ_000543的表达。运用SPSS 20.0分析hsa_circ_000543表达与宫颈癌患者临床特征的相关性。将hsa_circ_000543的上调或下调质粒分别转染至宫颈癌细胞中。分别通过CCK-8检测、流式细胞术和细胞集落形成实验检测细胞增殖、凋亡和集落形成情况。通过Transwell实验评估细胞迁移和侵袭能力。利用生物信息学预测工具和荧光素酶报告基因实验研究hsa_circ_000543潜在的分子机制。进行挽救实验以验证hsa_circ_000543/miR-567/ZNF268轴在宫颈癌中的调控机制。
hsa_circ_000543在宫颈癌组织和细胞中高表达。hsa_circ_000543高表达提示宫颈癌患者预后不良。hsa_circ_000543促进宫颈癌细胞增殖、集落形成、迁移和侵袭，并抑制细胞凋亡。在宫颈癌细胞系中，hsa_circ_000543直接靶向miR-567/ZNF268。在宫颈癌肿瘤组织和细胞中，hsa_circ_000543表达与miR-567表达呈负相关，与ZNF268表达呈正相关。挽救实验表明，hsa_circ_000543通过调控miR-567/ZNF268轴介导宫颈癌细胞的增殖、凋亡、集落形成、迁移和侵袭。
hsa_circ_000543通过结合miR-567并增强ZNF268表达来调控宫颈癌细胞活性。
