Dexian Wei1, Meirong Tian2, Weibo Fan3, Xiaojing Zhong1, Shuhong Wang1, Yahang Chen4, Shihong Zhang5. 1. Department of Obstetrics, Penglai People's Hospital, Penglai City, Shandong Province, China. 2. Department of Obstetrics, Shandong Maternal and Child Health Hospital Affiliated of Shandong University, Jinan City, Shandong Province, China. 3. Department of Obstetrics and Gynecology, Shouyi Maria Maternity Hospital, Wuhan City, Hubei Province, China. 4. Department of Obstetrics and Gynecology, Heilongjiang Provincial Hospital, No.82 Zhongshan Road, Xiangfang District, Haerbin City, 150036, Heilongjiang Province, China. devqgg@163.com. 5. Department of Obstetrics, West China Second Hospital, Sichuan University, South gaden, Zhongyuan lane, Section 4, Renmin south road, Wuhou district, Chengdu City, 610041, Sichuan Province, China. aevssa@163.com.
Abstract
BACKGROUND: Circular RNAs (circRNAs) are involved in a variety of biological processes, including tumorigenesis. However, the exact role and molecular mechanisms of circ_0000043 in endometrial carcinoma (EC) remain largely unknown. METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was carried out to determine the expression levels of circ_0000043, microRNA-1271-5p (miR-1271-5p) and catenin delta 1 (CTNND1). 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry were used to measure cell proliferation, cell apoptosis and cell cycle distribution, respectively. Cell migration and invasion were assessed by transwell assay. Western blot assay was performed to examine the protein expression of matrix metalloproteinase 2 (MMP2), MMP9 and CTNND1. The interaction between miR-1271-5p and circ_0000043 or CTNND1 was predicted by starBase and confirmed by dual-luciferase reporter assay. The mice xenograft model was established to investigate the role of circ_0000043 in vivo. RESULTS: Circ_0000043 and CTNND1 were highly expressed and miR-1271-5p was lowly expressed in EC tissues and cells. Knockdown of circ_0000043 inhibited the progression of EC by inhibiting cell proliferation, migration, invasion and tumor growth (in vivo) and promoting apoptosis. MiR-1271-5p was a direct target of circ_0000043 and its inhibition reversed the inhibitory effect of circ_0000043 knockdown on the progression of EC cells. In addition, CTNND1 was a downstream target of miR-1271-5p, and miR-1271-5p overexpression inhibited EC cell proliferation, migration and invasion and induced apoptosis by targeting CTNND1. Moreover, circ_0000043 positively regulated CTNND1 expression by sponging miR-1271-5p. CONCLUSION: Circ_0000043 knockdown inhibited the progression of EC by regulating miR-1271-5p/CTNND1 axis, which might provide a promising circRNA-targeted therapy for EC.
BACKGROUND: Circular RNAs (circRNAs) are involved in a variety of biological processes, including tumorigenesis. However, the exact role and molecular mechanisms of circ_0000043 in endometrial carcinoma (EC) remain largely unknown. METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was carried out to determine the expression levels of circ_0000043, microRNA-1271-5p (miR-1271-5p) and catenin delta 1 (CTNND1). 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry were used to measure cell proliferation, cell apoptosis and cell cycle distribution, respectively. Cell migration and invasion were assessed by transwell assay. Western blot assay was performed to examine the protein expression of matrix metalloproteinase 2 (MMP2), MMP9 and CTNND1. The interaction between miR-1271-5p and circ_0000043 or CTNND1 was predicted by starBase and confirmed by dual-luciferase reporter assay. The mice xenograft model was established to investigate the role of circ_0000043 in vivo. RESULTS: Circ_0000043 and CTNND1 were highly expressed and miR-1271-5p was lowly expressed in EC tissues and cells. Knockdown of circ_0000043 inhibited the progression of EC by inhibiting cell proliferation, migration, invasion and tumor growth (in vivo) and promoting apoptosis. MiR-1271-5p was a direct target of circ_0000043 and its inhibition reversed the inhibitory effect of circ_0000043 knockdown on the progression of EC cells. In addition, CTNND1 was a downstream target of miR-1271-5p, and miR-1271-5p overexpression inhibited EC cell proliferation, migration and invasion and induced apoptosis by targeting CTNND1. Moreover, circ_0000043 positively regulated CTNND1 expression by sponging miR-1271-5p. CONCLUSION: Circ_0000043 knockdown inhibited the progression of EC by regulating miR-1271-5p/CTNND1 axis, which might provide a promising circRNA-targeted therapy for EC.
Authors: Leslie S Bradford; Jose Alejandro Rauh-Hain; John Schorge; Michael J Birrer; Don S Dizon Journal: Am J Clin Oncol Date: 2015-04 Impact factor: 2.339
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