Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Harbin Medical University, Xuefu Road, Harbin 150086, PR China.
Department of Reproductive Endocrinology, Women's Hospital, Zhejiang University School of Medicine, Xueshi Road, Hangzhou, 310000, PR China.
Biomed Pharmacother. 2020 May;125:109965. doi: 10.1016/j.biopha.2020.109965. Epub 2020 Feb 10.
Cervical cancer (CC) is one of the most common cancers in women. Long non-coding RNAs (lncRNAs) have been proposed as therapeutic targets in CC. Hence, the present study evaluated the effect of ASB16-AS1 on CC via regulating miR-1305.
Differentially expressed lncRNAs associated with CC were screened using bioinformatics database. The expression of ASB16-AS1 and miR-1305 were measured by qRT-PCR in CC tissues and CC cells. Cell proliferation was assessed by CCK-8 and colon formation assays. Cell abilities of migration and invasion were detected by Transwell migration and invasion assays. Luciferase report assays were used to explore the correction between ASB16-AS1, miR-1305 and Wnt2 in CC. Western blot assay detect the activity of Wnt/β-catenin pathway. The xenograft tumor in nude mice was observed to evaluate tumor formation in vivo.
In our study, we showed that the expression of ASB16-AS1 was increased while miR-1305 reduced was re in CC. Clinically, ASB16-AS1 and miR-1305 were correlated with poor-associated clinicopathological features of CC patients. Knockdown of ASB16-AS1 reduced CC cells proliferation, migration and invasion abilities by regulating miR-1305 in vitro and in vivo. Moreover, miR-1305 was directly bound to ASB16-AS1 and Wnt2, regulated their expression negatively. Western blot assays showed that ASB16-AS1 functioned as an oncogene by Wnt/β-catenin pathway.
This study reveals that ASB16-AS1 promotes cell proliferation, migration, invasion via binding miR-1305 with Wnt2, and enhancing the Wnt/β-catenin pathway. ASB16-AS1 may play a new therapeutic target for CC.
宫颈癌（CC）是女性最常见的癌症之一。长链非编码 RNA（lncRNA）已被提出作为 CC 的治疗靶点。因此，本研究通过调节 miR-1305 来评估 ASB16-AS1 对 CC 的影响。
使用生物信息学数据库筛选与 CC 相关的差异表达 lncRNA。通过 qRT-PCR 测量 CC 组织和 CC 细胞中 ASB16-AS1 和 miR-1305 的表达。通过 CCK-8 和结肠形成测定评估细胞增殖。通过 Transwell 迁移和侵袭测定检测细胞迁移和侵袭能力。荧光素酶报告测定用于探索 CC 中 ASB16-AS1、miR-1305 和 Wnt2 之间的纠正关系。Western blot 测定检测 Wnt/β-catenin 通路的活性。裸鼠体内异种移植瘤观察体内肿瘤形成。
在我们的研究中，我们表明 ASB16-AS1 的表达增加，而 miR-1305 的表达减少在 CC 中。临床上，ASB16-AS1 和 miR-1305 与 CC 患者不良相关的临床病理特征相关。体外和体内敲低 ASB16-AS1 通过调节 miR-1305 降低 CC 细胞的增殖、迁移和侵袭能力。此外，miR-1305 直接与 ASB16-AS1 和 Wnt2 结合，负调控它们的表达。Western blot 测定表明，ASB16-AS1 通过 Wnt/β-catenin 通路发挥癌基因作用。
这项研究表明，ASB16-AS1 通过与 Wnt2 结合并增强 Wnt/β-catenin 通路来促进细胞增殖、迁移和侵袭。ASB16-AS1 可能成为 CC 的新治疗靶点。
