MicroRNA-1324 inhibits cell proliferative ability and invasiveness by targeting MECP2 in gastric cancer

X.-Y. Zhang, Y.-Y. Xu, W.-Y. Chen

Department of Gastrointestinal and Colorectal Surgery, China-Japan Union Hospital of Jilin University, Changchun, China. 776726739@qq.com

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• Oncology

OBJECTIVE: The aim of this study was to investigate the expression level and potential molecular mechanism of microRNA-1324 in gastric cancer (GCa) to provide a new perspective for the diagnosis and treatment of GCa.

PATIENTS AND METHODS: The expression levels of microRNA-1324 and MECP2 in GCa tissues and cell lines were detected using quantitative Real Time Polymerase Chain Reaction (qRT-PCR). The influence of microRNA-1324 and MECP2 on the proliferation or invasiveness of GCa cells were investigated by cell counting kit-8 (CCK-8) and colony formation assay or transwell assay, respectively. Furthermore, the regulatory interplay between microRNA-1324 and MECP2 was verified via Dual-Luciferase reporting assay, qRT-PCR, and Western Blot.

RESULTS: QRT-PCR results revealed that microRNA-1324 expression was remarkably down-regulated in GCa tissues and cell lines, while the expression of MECP2 was remarkably up-regulated. Subsequently, we confirmed that miR-1324 could target and bind to MECP2, as well as inhibit its expression. Inhibition of microRNA-1324 remarkably enhanced the proliferative capacity and invasiveness of GCa cells. However, opposite results were observed after inhibiting MECP2 expression. At the same time, flow cytometry revealed that inhibition of microRNA-1324 accelerated cell cycle but inhibited apoptosis. Conversely, opposite results were observed when MECP2 was down-regulated in vitro.

CONCLUSIONS: MicroRNA-1324 was remarkably down-regulated in GCa tissues or cell lines. Meanwhile, it could inhibit MECP2 expression, and promote the proliferation and invasion of GCa cells, eventually participating in the occurrence and development of GCa.

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