[No authors listed]
Long nonâcoding RNAs (lncRNAs) serve a crucial role in gastric cancer (GC) progression. However, the molecular mechanism underlying lncRNA JPX transcript, XIST activator (JPX) in the tumorigenesis of GC is not completely understood. Reverse transcriptionâquantitative PCR (RTâqPCR) and western blotting were performed to detect gene expression. A luciferase reporter gene assay was conducted to determine the relationship between microRNA (miR)â197 and JPX or CâXâC motif chemokine receptor 6 (CXCR6). Cell viability, migration and invasion were determined by performing MTT, wound healing and Transwell assays, respectively. The Cancer Genome Atlas database and the RTâqPCR results indicated that JPX expression was upregulated and miRâ197 expression was downregulated in patients with GC and in GC cells. Moreover, high JPX expression and low miRâ197 expression in patients with GC indicated poor prognosis. miRâ197 expression was directly inhibited by JPX. Compared with the short hairpin RNA (sh) negative control (NC) group, NCIâN87 and MKNâ45 cells in the shJPX group displayed decreased cell viability and invasion, as well as a wider scratch width. NCIâN87 and MKNâ45 cells in the shJPX + miRâ197 inhibitor group had increased viability and invasion, but a narrower scratch width compared with the shJPX group. It was also identified that miRâ197 directly inhibited CXCR6 expression. miRâ197 inhibited Beclin1 protein expression and promoted p62 protein expression. Compared with the NC group, NCIâN87 and MKNâ45 cells in the miRâ197 mimic group had decreased cell viability and invasion, and a wider scratch width. Enhanced cell viability and invasion, and a narrower scratch width was also observed in the miRâ197 mimic + CXCR6 and miRâ197 mimic + Beclin1 groups, compared with the miRâ197 mimic group. Collectively, the results indicated that lncRNA JPX promoted GC progression by regulating CXCR6 and autophagy via inhibiting miRâ197. Furthermore, JPX knockdown regulated GC cell phenotype by promoting miRâ197.
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