Abstract
BackgroundGastric carcinoma (GC) ranks the fifth most common cancer worldwide, with high incidence and mortality rates. Numerous microRNAs (miRNAs), including miR-654-5p, have been implicated in the pathophysiological processes of tumorigenesis. Nevertheless, the mechanism of miR-654-5p in GC is unclear.ObjectivesOur study is devoted to exploring the function and molecular mechanism of miR-654-5p on the malignant cell behaviors of GC.MethodsThe gene expression was detected by reverse transcription quantitative polymerase chain reaction. GC cell proliferation and motion were assessed by colony formation assay and transwell assay. The binding capacity between miR-654-5p and G protein-regulated inducer of neurite outgrowth 1 (GPRIN1) was explored by luciferase reporter and RNA pulldown assays. The protein levels were detected by Western blotting.ResultsmiR-654-5p expression was higher in GC cells and tissues than control cells and tissues. miR-654-5p promoted GC cell growth and motion. Moreover, our findings showed that miR-654-5p was bound with GPRIN1. Importantly, downregulation of GPRIN1 rescued the inhibitory influence of miR-654-5p knockdown on GC cell malignant behaviors. Additionally, miR-654-5p activated the nuclear factor kappa-B (NF-κB) pathway by regulation of GPRIN1.ConclusionsmiR-654-5p facilitated cell proliferation, migration, and invasion in GC via targeting the GPRIN1 to activate the NF-κB pathway.
Highlights
Gastric carcinoma (GC) is one of the most common malignant tumors worldwide due to its high incidence and mortality rates [1]
G protein-regulated inducer of neurite outgrowth 1 (GPRIN1) was proved to be a vital regulator in numerous human cancers, its role in GC remains unclear yet
A negative expression correlation between miR-654-5p and GPRIN1 was observed in 36 collected GC tissues (Figure 3d). miR654-5p was overexpressed in GC cells compared to that in normal cells (Figure 3e)
Summary
Gastric carcinoma (GC) is one of the most common malignant tumors worldwide due to its high incidence and mortality rates [1]. Every year about one million people are diagnosed with gastric cancer all over the world, of whom about three quarters die from this horrible disease [2]. The incidence rates of GC vary significantly between different genders and across different countries [3]. Despite greatly improved GC treatments, the prognosis is still unsatisfactory. The overall 5-year survival rate and disease-free rate are very low in most areas of the world [4]. Exploring the molecular basis of GC is essential for developing novel therapeutic treatments to improve the current poor survival rate
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