miR-876-5p通过负反馈调节上皮-间质样转化在胃癌进展中的作用及机制研究

doi:10.3969/j.issn.1006-6233.2023.06.01

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Abstract Objective: To explore the effect and mechanism of miR-876-5p regulating epithelial-mesenchymal transition (EMT) on the progression of gastric cancer. Methods: The differences in miR-876-5p expression in gastric cancer tissues and normal tissues adjacent to the cancer were determined by real-time fluorescence quantitative PCR; gastric cancer cells were divided into control group, EMT group, miR-NC+EMT group, miR-876-5p+EMT group, miR-876-5p+EMT+isoproterenol hydrochloride (ISO) group, miR-NC or miR-876-5p were transfected into gastric cancer cells according to the grouping, and 5 ng/mL transforming growth factor-β (TGF-β1) was induced for 24 h to establish an EMT model of gastric cancer cells and 20 μmol/L extracellular. After treatment, the expression of E-cadherin, N-cadherin and vimentin was detected by immunofluorescence staining in each group of cells, and the expression of E-cadherin, Vimentin, N-cadherin, matrix metalloproteinase-2 (MMP-2) and MMP-9 protein was determined by protein immunoblotting (Western blot) in each group of cells. The expression of E-cadherin, Vimentin, N-cadherin, Snail, matrix metalloproteinase-2 (MMP-2) and MMP-9 in each group of cells was determined by western blot. Western blot was performed to determine the expression of ERK signaling pathway-related proteins in each group of cells. Results: The relative expression of miR-876-5p was decreased in gastric cancer tissues compared with normal tissues next to cancer (P<0.05); compared with the EMT group, the fluorescence expression of E-cadherin was enhanced and that of Vimentin and N-cadherin was decreased in the miR-876-5p+EMT group of gastric cancer cells, and the relative expression of E-cadherin protein was upregulated while Vimentin, N-cadherin, Snail, MMP-2, and MMP-9 protein relative expression were all downregulated (P<0.05), cell proliferation activity and EdU positivity were reduced (P<0.05), migration number and invasion number were decreased (P<0.05), and p-ERK1/2 protein relative expression was downregulated (P<0.05); while with miR-876-5p+EMT group, E-cadherin fluorescence expression was diminished, Vimentin and N-cadherin fluorescence expression was enhanced, E-cadherin protein relative expression was down-regulated, and Vimentin, N-cadherin, Snail, MMP- 2, MMP-9 protein relative expression were upregulated (P<0.05), cell proliferation activity and EdU positivity were increased (P<0.05), migration number and invasion number were increased (P<0.05), while p-ERK1/2 protein relative expression was upregulated (P<0.05). Conclusion: miR-876-5p affects tumor progression by regulating the EMT process in gastric cancer cells, and this effect may be related to the inhibition of TGF-β1-mediated activation of the ERK signaling pathway.

Key words： Gastric cancer miR-876-5p Epithelial-mesenchymal transition Extracellular signal-regulated kinase signaling pathway

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	CUI Qin
	ZHAO Cuijuan
	QU Zhenjie

Cite this article:

CUI Qin,ZHAO Cuijuan,QU Zhenjie. The Role and Mechanism of miR-876-5p in the Progression of Gastric Cancer by Regulating Epithelial-Mesenchymal Transition through Negative Feedback[J]. HeBei Med, 2023, 29(6): 881-886.

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http://www.hbyxzzs.cn/EN/10.3969/j.issn.1006-6233.2023.06.01 OR http://www.hbyxzzs.cn/EN/Y2023/V29/I6/881

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