Wei Liu1, Rujin Zhuang2, Shujun Feng3, Xiaoxu Bai4, Zhaoyang Jia5, Elena Kapora6, Wenhua Tan7. 1. Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Harbin Medical University, Xuefu Road, Harbin 150086, PR China. Electronic address: liuwei1978@163.com. 2. Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Harbin Medical University, Xuefu Road, Harbin 150086, PR China. Electronic address: zhangrujin@163.com. 3. Department of Reproductive Endocrinology, Women's Hospital, Zhejiang University School of Medicine, Xueshi Road, Hangzhou, 310000, PR China. Electronic address: fsj1-1@163.com. 4. Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Harbin Medical University, Xuefu Road, Harbin 150086, PR China. Electronic address: Baixxx@163.com. 5. Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Harbin Medical University, Xuefu Road, Harbin 150086, PR China. Electronic address: jiazhaoyang@126.com. 6. Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Harbin Medical University, Xuefu Road, Harbin 150086, PR China; Central Laboratory of Scientific Research, Bashkir State Medical University, Lenina Street; Ufa, 450008, Russian Federation. Electronic address: caporix@yandex.ru. 7. Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Harbin Medical University, Xuefu Road, Harbin 150086, PR China. Electronic address: 13766800936@139.com.
Abstract
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.