Circular RNA hsa_circ_0030018 acts as a sponge of miR-599 to aggravate esophageal carcinoma progression by regulating ENAH expression |
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Authors: | Chengxiang Wang Derong Tang Hongying Wang Guodong Hu Shuo Hu Lei Li Bo Min Yaqin Wang |
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Affiliation: | 1. Department of Thoracic Surgery, Huai'an Second People's Hospital, The Affiliated Huai'an Hospital of Xuzhou Medical University, Huaian, Jiangsu, China;2. The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huaian, Jiangsu, China |
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Abstract: | Esophageal carcinoma (EC) bears one of the most rapid-growing incidences in cancers, which also has the highest mortality rate worldwide. Multiple studies have authenticated that circular RNAs (circRNAs) significantly work on the progression of cancers. circRNA hsa_circ_0030018 was also verified to exert functions on the development of glioma previously. Nevertheless, the biological function of hsa_circ_0030018 in EC has not been well elucidated yet. In the present study, the results displayed the expression of hsa_circ_0030018 was dramatically increased in EC cells. Inhibition of has_circ_0030018 suppressed cell proliferation, migration, and epithelial-mesenchymal transition (EMT) process in EC. Based on molecular mechanism assays, has_circ_0030018 served as a sponge of miR-599. Enabled homolog (ENAH), which exhibited high expression in EC cells, was confirmed to be a downstream target gene of miR-599. Additionally, has_circ_0030018 positively regulated ENAH expression while miR-599 negatively regulated ENAH expression. Finally, by employing rescue assays, ENAH deficiency partially counteracted the promoting function of miR-599 silence on cell proliferation, migration, and EMT process in EC cotransfected with sh- has_circ_0030018#1 cells. In conclusion, hsa_circ_0030018 acted as a sponge of miR-599 to aggravate EC progression by regulating ENAH expression. Therefore, hsa_circ_0030018 might serve as a promising biomarker and therapeutic target for EC. |
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Keywords: | ENAH esophageal carcinoma hsa_circ_0030018 miR-599 |
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