Abstract
Gastric cancer (GC) is one of the most common cancers, with high incidences in East Asia. microRNAs (miRNAs) play essential roles in the carcinogenesis of GC. miR-20a was elevated in GC, while the potential function of miR-20a was poorly understood. miR-20a expression was examined in GC tissues and cell lines. The effects of miR-20a on the growth, migration, invasion, and chemoresistance of GC cells were examined. Luciferase reporter assay and Western blot were used to screen the target of miR-20a. miR-20a was increased in GC tissues and cell lines. miR-20a promoted the growth, migration and invasion of GC cells, enhanced the chemoresistance of GC cells to cisplatin and docetaxel. Luciferase activity and Western blot confirmed that miR-20a negatively regulated EGR2 expression. Overexpression of EGR2 significantly attenuated the oncogenic effect of miR-20a. miR-20a was involved in the carcinogenesis of GC through modulation of the EGR2 signaling pathway.
Highlights
Gastric cancer (GC) is one of the most common cancers and the second most common malignancy of cancer death worldwide, especially in East Asia [1]
We explored the biological effects and the potential mechanisms of miR-20a in GC by detecting the expression of miR-20a in GC, validating previous finding that miR-20a was elevated in GC
A recent study suggested that miR-20a overexpression in rheumatoid fibroblast-like synoviocytes decreased apoptosis signal-regulating kinase 1 (ASK1) activity, indicating an anti-apoptotic effect [22]. miR-20a was up-regulated in gallbladder carcinoma [23], but down-regulated in hepatocellular carcinoma [24]
Summary
Gastric cancer (GC) is one of the most common cancers and the second most common malignancy of cancer death worldwide, especially in East Asia [1]. MiRNAs functioned as oncogenes or tumor suppressors by regulating different target gene expression in different cancers. MiR-9, miR-22, and miR-146a had all been shown to act as tumor suppressors [9,10,11], whereas miR-19, miR-23a, and miR-301a had been shown to function as oncogenes [12,13,14]. These studies suggested that dysregulation of miRNAs might be involved in carcinogenesis and cancer progression. Overexpression of EGR2 significantly attenuated the oncogenic effect of miR-20a
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