RETRACTED: MiR-143-3p functions as a tumor suppressor by regulating cell proliferation, invasion and epithelial-mesenchymal transition by targeting QKI-5 in esophageal squamous cell carcinoma (Retracted article. See vol. 21, 2022)

被引:132
作者
He, Zhenyue [1 ]
Yi, Jun [2 ]
Liu, Xiaolong [2 ]
Chen, Jing [1 ]
Han, Siqi [1 ]
Jin, Li [1 ]
Chen, Longbang [1 ]
Song, Haizhu [1 ]
机构
[1] Nanjing Univ, Jinling Hosp, Dept Med Oncol, Sch Med, 305 Zhongshan East Rd, Nanjing 210002, Jiangsu, Peoples R China
[2] Nanjing Univ, Jinling Hosp, Dept Cardiothorac Surg, Sch Med, 305 Zhongshan East Rd, Nanjing 210002, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
MiR-143-3p; Esophageal squamous cell carcinoma; QKI-5; Proliferation; Invasion; RNA-BINDING PROTEIN; GASTRIC-CANCER; QUAKING; PROMOTES; GROWTH; MICRORNA-155; EXPRESSION; APOPTOSIS;
D O I
10.1186/s12943-016-0533-3
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Background: Dysregulation of microRNAs (miRNAs) have been demonstrated to contribute to carcinogenesis. MiR-143-3p has been identified to function as a tumor suppressor in several tumors, but the role of miR-143-3p in esophageal squamous cell carcinoma (ESCC) has not been intensively investigated. Our aim was to evaluate the potential role of miR-143-3p in the progression of ESCC. Methods: The expression levels of miR-143-3p and QKI-5 protein were measured in 80 resected ESCC tumor specimens and the clinicopathological significance of these levels determined. We also investigated the role of miR-143-3p in the regulation of QKI-5 expression in ESCC cell lines both in vivo and in vitro. Results: MiR-143-3p levels were decreased in ESCC clinical samples and low expression of miR-143-3p was significantly associated with poor prognosis in ESCC patients. Ectopic expression of miR-143-3p suppressed proliferation and induced apoptosis in ESCC cells both in vivo and in vitro. Ectopic expression of miR-143-3p also reduced the metastatic potential of cells by selectively regulating epithelial-mesenchymal transition regulatory proteins. Furthermore, QKI-5 isoform was upregulated in ESCC tissues and was a direct target of miR-143-3p. Lastly, re-introduction of QKI-5 expression abrogated the inhibitory effects of miR-143-3p on ESCC cell proliferation and motility. Conclusions: Our results demonstrate that miR-143-3p acts as a tumor-suppressor by targeting QKI-5 in ESCC, suggesting that miR-143-3p is a potential therapy for the treatment of ESCC.
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页数:17
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