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miRNA‑183‑5p.1 promotes the migration and invasion of gastric cancer AGS cells by targeting TPM1.

Oncol Rep. 2019 Dec;42(6):2371-2381. doi:10.3892/or.2019.7354. Epub 2019 Oct 04
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摘要


MicroRNA‑183 (miR‑183) is a small, non‑coding RNA that is involved in post‑transcriptional processes, is upregulated in gastric cancer and acts as an oncogene in cancer migration. Although fragmentary reports have demonstrated the importance of miR‑183 in gastric cancer, its biofunctions and regulatory effects are still unknown. In the present study, the gene and protein expression levels were determined by reverse transcription‑quantitative PCR and western blot analysis. The connection between miR‑183‑5p.1 and tropomyosin 1 (TPM1) was tested through luciferase reporter experiments. Cell viability, apoptosis and related proteins were detected by MTT assay, flow cytometry, immunofluorescence and western blotting, respectively. The migration and invasion of AGS cells modulated by miR‑183‑5p.1 were analyzed by Transwell assay. TPM1 expression was found to be decreased in gastric cancer tissues and cell lines when compared with normal and adjacent tissues and gastric epithelial cells, and was regulated by miR‑183‑5p.1 targeting TPM1. miR‑183‑5p.1 overexpression facilitated the growth and suppressed the death of AGS cells through Bcl‑2 and P53 proteins. In addition, miR‑183‑5p.1 restricted TPM1, TPM2 and TPM3 protein expression in AGS cells. The excessive levels of miR‑183‑5p.1 promoted the migration and invasion of AGS cells, and inhibited the apoptosis of AGS cells. However, the knockdown of miR‑183‑5p.1 induced the opposite in AGS cells. In conclusion, miR‑183‑5p.1 promotes cell proliferation, migration and invasion by downregulating TPM1 and deactivating the Bcl‑2/P53 signaling pathways in gastric cancer, indicating that miR‑183‑5p.1 and TPM1 may be potential targets for the diagnosis or therapy of gastric cancer in the future.

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