Abstract
Esophageal cancer (ECa) remains a major cause of mortality across the globe. The expression of EIF3J-AS1 is altered in a plethora of tumors, but its role in ECa development and progression are undefined. Here, we show that EIF3J-AS1 is up-regulated in ECa and that its expression correlates with advanced TNM stage (P = 0.014), invasion depth (P = 0.001), positive lymph node metastasis (P < 0.001) and poor survival (OS: P = 0.0059; DFS: P = 0.0037) in ECa. Functional experiments showed that knockdown EIF3J-AS1 inhibited ECa growth and metastasis through in vitro and in vivo experiments. Regarding the mechanism, EIF3J-AS1/miR-373-3p/AKT1 established the ceRNA network involved in the modulation of cell progression of ECa cells. Overall, EIF3J-AS1 may exhibit an oncogenic function in ECa via acting as a sponge for miR-373-3p to up-regulate AKT1 mRNA level, and may serve as a potential therapeutic target and a prognostic biomarker for ECa patients.
Highlights
Esophageal cancer (ECa) remains a major cause of mortality across the globe
RT-PCR analysis further showed that EIF3J-AS1 was up-regulated in ECa cell lines vs. non-ECa HECC cells
The dysregulation of lncRNAs is increasing linked to tumorigenesis, with both oncogenic and tumor suppressor functions reported[22,23,24,25]
Summary
Esophageal cancer (ECa) remains a major cause of mortality across the globe. The expression of EIF3J-AS1 is altered in a plethora of tumors, but its role in ECa development and progression are undefined. EIF3J-AS1 may exhibit an oncogenic function in ECa via acting as a sponge for miR-373-3p to up-regulate AKT1 mRNA level, and may serve as a potential therapeutic target and a prognostic biomarker for ECa patients. Diagnostic and therapeutic advances have been made to improve ECa therapeutics, including biopsies, chromo endoscopy and narrow-band imaging[2] Despite these improvements, the efficiency of ECa therapies and subsequent patient prognosis remains poor. ECa remains a global health burden for which new diagnostics and effective therapeutic strategies are urgently required[3]. We examined the increased expression of EIF3J-AS1 in ECa cell lines and tissues, the effect of EIF3J-AS1 knocked down on inhibiting the metastasis and growth of ECa cell lines in vitro and vivo. We examined the role of EIF3J-AS1 in ECa cells’ aggressive phenotypes by miR-373-3p binding and assessing the AKT1 expression
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