Down-Regulation of miR-2053 Inhibits the Development and Progression of Esophageal Carcinoma by Targeting Fyn-Related Ki
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ORIGINAL ARTICLE
Down‑Regulation of miR‑2053 Inhibits the Development and Progression of Esophageal Carcinoma by Targeting Fyn‑Related Kinase (FRK) Bin Wang1 · Li Zhang2 · Jindong Li1 · Peiyan Hua1 · Yan Zhang1 Received: 22 August 2019 / Accepted: 12 December 2019 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Background MicroRNAs (miRNAs) play essential roles in the regulation and pathophysiology of various types of cancers including esophageal carcinoma (ESCA). Increasing numbers of miRNAs have been identified to be important regulators in the progression of ESCA by regulating gene expression. However, functional miRNAs and the underlying mechanisms involved in ESCA need sufficient elucidation. Aims In the present study, the function of miR-2053 was investigated in ESCA cells. Methods The expression of miR-2053 was detected in four different ESCA cell lines (Eca109, Ec9706, KYSE30, and TE-1 cells) and normal cell line (HEEC) by qRT-PCR. Cell proliferation, migration, and invasion abilities after knockdown of miR-2053 were assessed by CCK-8 assay, scratch assay, and transwell assay, respectively. Cell cycle of ESCA cells was detected by flow cytometric analysis. Expression of proteins in ESCA cells was detected by Western blot analysis. Results The results showed that the expression of miR-2053 was remarkably up-regulated in ESCA tissues and cells lines. Down-regulation of miR-2053 markedly inhibited cell proliferation, migration, and invasion and markedly induced cell cycle arrest and cell apoptosis in ESCA cell lines. Fyn-related kinase (FRK) was a target gene of miR-2053. Moreover, down-regulation of miR-2053 mediated the protein kinase B (AKT)/mammalian target of rapamycin and Wnt3a/β-catenin signaling pathway in ESCA cell lines. Conclusions Our results together suggest the potential of regulating miR-2053 expression against development and progression of esophageal carcinoma by targeting FRK. Keywords miR-2053 · ESCA · FRK · AKT/mTOR · Wnt/β-catenin
* Yan Zhang [email protected] Bin Wang [email protected] Li Zhang [email protected] Jindong Li [email protected] Peiyan Hua [email protected] 1
Department of Thoracic Surgery, The Second Hospital of Jilin University, No. 218 Ziqiang Street, Changchun City 130041, Jilin Province, People’s Republic of China
Department of Anesthesiology, The Second Hospital of Jilin University, Changchun City 130041, Jilin Province, People’s Republic of China
2
Introduction Esophageal carcinoma (ESCA) is a common but life-threatening disease ranking the seventh main cause of cancerinduced death around the world, and its pathogenesis is complicated [1]. The diagnosis of ESCA is usually delayed with poor treatment responses, and the 5-year relative survival rate is only 4% in late-diagnosed patients [2, 3]. Therefore, comprehensive elucidation of the molecular mechanisms underlying the complex process of ESCA is of great significance for seeking novel therapeutic approaches and so early diagnosis and tr
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