Circ_0096710 facilitates tumor growth via controlling ADAM10 expression in esophageal squamous cell carcinoma

Circ_0096710 通过控制食管鳞状细胞癌中的 ADAM10 表达促进肿瘤生长

阅读:3
作者:Chaoqun Dong, Zhilong Li

Background

Esophageal squamous cell carcinoma (ESCC) is a global cancer related to the sixth largest cause of death. Circular RNAs (circRNAs) have affected the progress of ESCC during recent years, but the mechanism is not completely clear. So here we probed the effects of hsa_circ_0096710 (circ_0096710) in ESCC.

Conclusion

Circ_0096710 upregulates ADAM10 via mediating miR-1294 expression so as to accelerate the occurrence of ESCC, suggesting that circ_0096710 may be a potential therapeutic target for ESCC.

Methods

Relative levels of circ_0096710, miR-1294, and ADAM10 were quantified by the quantitative real-time reverse transcription-polymerase chain reaction in ESCC tissues. Western blot assessed ADAM10, PCNA, MMP2, VEGFA, and OCT4 protein levels. Cell proliferative capacity was assessed by cell counting and cell colony-forming assays. Transwell assays assessed cell migration and invasion. Angiogenesis was detected by tube formation assays. Stemness of cancer cells was estimated by sphere formation assays. Dual-luciferin reporter and RNA immunoprecipitation assays determined the targeting relationship between miR-1294 and circ_0096710 or ADAM10.

Results

Relative levels of circ_0096710 and ADAM10 mRNA were upregulated in ESCC cells, yet miR-1294 was downregulated. Circ_0096710 silencing repressed ESCC cell proliferation, migration, invasion, angiogenesis, and stem-like properties. Moreover, circ_0096710 was an upstream target of miR-1294, and miR-1294 inhibition reversed the role of circ_0096710 downregulation in ESCC cells. Furthermore, ADAM10 was a downstream target of miR-1294, and miR-1294 overexpression suppressed ESCC cell proliferation, migration, invasion, angiogenesis, and stem-like properties by targeting ADAM10. Meanwhile, circ_0096710 upgraded ADAM10 expression through sponging miR-1294. Also, circ_0096710 downregulation restrained tumor growth in mouse models.

特别声明

1、本文转载旨在传播信息,不代表本网站观点,亦不对其内容的真实性承担责任。

2、其他媒体、网站或个人若从本网站转载使用,必须保留本网站注明的“来源”,并自行承担包括版权在内的相关法律责任。

3、如作者不希望本文被转载,或需洽谈转载稿费等事宜,请及时与本网站联系。

4、此外,如需投稿,也可通过邮箱info@biocloudy.com与我们取得联系。