Abstract
BackgroundIncreasing evidence shows that stimulated by retinoic acid 6 (STRA6) participates in regulating multiple cancers. However, the biological roles of STRA6 in gastric cancer (GC) remain unknown. This study aimed to investigate the biological function of STRA6 and reveal the underlying mechanism of its dysregulation in GC.MethodsThe expression level of STRA6 was detected through quantitative real-time PCR and Western blot analysis. The effects of STRA6 on the proliferation of GC cells were studied through CCK-8 proliferation, colony formation and 5-ethynyl-2′-deoxyuridine (EdU) assays. The effects of STRA6 on migration and invasion were detected via wound healing and Transwell assays. Upstream miRNAs, which might regulate STRA6 expression, was predicted through bioinformatics analysis. Their interaction was further confirmed through dual-luciferase reporter assays and rescue experiments.ResultsSTRA6 was up-regulated in GC and enhanced the proliferation and metastasis of GC cells in vitro and in vivo. STRA6 knockdown could inhibit the Wnt/β-catenin signalling pathway. STRA6 was confirmed as an miR-873 target, which acted as a tumour suppressor in GC. Rescue assays showed that the repressing effect of miR-873 could be partially reversed by overexpressing STRA6.ConclusionsSTRA6 is down-regulated by miR-873 and plays an oncogenic role by activating Wnt/β-catenin signalling in GC.
Highlights
Increasing evidence shows that stimulated by retinoic acid 6 (STRA6) participates in regulating multiple cancers
The expression levels of STRA6 in 80 pairs of gastric cancer (GC) and adjacent normal tissues, GC cell lines (MKN45, MGC803, BGC823 and SGC7901) and GES-1 were measured via Quantitative real-time PCR (qRT-PCR)
These findings showed that STRA6 was up-regulated in GC and had a therapeutic potential for patients with GC
Summary
Increasing evidence shows that stimulated by retinoic acid 6 (STRA6) participates in regulating multiple cancers. The biological roles of STRA6 in gastric cancer (GC) remain unknown. Gastric cancer (GC) remains a prevalent malignancy worldwide. It was responsible for over 1000,000 new cases in 2018 and approximately 783,000 deaths, making it the fifth-most frequently diagnosed cancer and the third leading cause of cancer-related deaths [1]. The Cancer Genome Atlas (TCGA), a public database that has profiled and analysed large numbers of human tumours to discover molecular aberrations at DNA, RNA, protein and epigenetic levels [8, 9]. By screening the TCGA database, we found that the expression of stimulated by retinoic acid 6 (STRA6) is significantly aberrant between GC tissue and normal tissues. STRA6 mediates cellular retinol uptake and participates in retinyl ester accumulation in embryonic
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