The lncRNA XIST promotes proliferation, migration and invasion of gastric cancer cells by targeting miR-337

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Background and study aims: Gastric cancer (GC) is one of the most common malignant tumours worldwide. Long non-coding RNAs (lncRNAs) and microRNAs regulate the occurrence and development of various cancers and play an important role in GC progression. X-inactive specific transcript (XIST), a carcinogenic lncRNA, is involved in human tumourigenesis and is altered in GC. Janus kinase 2 (JAK2), a transcription factor, is involved in cancer cell metastasis and differentiation. However, the exact mechanism underlying the biological roles of XIST and JAK2 in cancer cells remains unclear. Material and methodsThis study was conducted using GES-1, HGC-27, AGS and HEK-293 T cells. Quantitative polymerase chain reaction and western blotting were performed to detect XIST, microRNA-337 (miR-337) and JAK2 expressions. GC cell invasion was investigated by using the Transwell assay. Fluorescein reporter gene detection was used to determine the relationship between JAK2 and XIST. ResultsCompared with that in GES-1 cells, XIST expression was significantly up-regulated in AGS and HGC-27 cells. miR-337 expression in GC cell lines was decreased. The proliferation, invasion and migration of GC cells were simultaneously inhibited by XIST knockdown, and the relationship between XIST and miR-337 was confirmed by bioinformatics analysis. JAK2 is expected to be the target gene of miR-337. MiR-337 can negatively regulate JAK2 expression in vitro. In addition, si-XIST decreased JAK2 expression by up-regulating miR-337 in vitro, thereby inhibiting GC cell proliferation and migration. Therefore, we speculated that XIST regulates JAK2 by competing with miR-337 as a competitive endogenous lncRNA in GC. ConclusionWe elucidated the effects of migration and invasion after XIST inhibition, at least in part, by inhibiting miR-337 expression in GC cells to regulate JAK2. These data indicate that a positive feedback loop exists between XIST and JAK2 and suggest that JAK2 and XIST play a vital role in cancer cell migration and invasion.