miR-484通过调控HIF-1α/VEGF信号通路对胃癌血管生成的影响<sup>*</sup>

doi:10.3969/j.issn.1671-7171.2024.09.003

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Abstract 【Objective】To investigate whether miR-484 participates in gastric cancer angiogenesis by regulating the HIF-1α/VEGF signaling pathway.【Methods】SCG-7901 gastric cancer cells were transfected with miR-NC, miR-484 mimics, and miR-484 inhibitors separately. The expression of hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) mRNA and protein, as well as the proliferation of gastric cancer cells, were measured in each group. The individual SCG-7901 cells with successfully transfected miR-NC,miR-484 mimics and miR-484 inhibitors were co-cultured with vascular endothelial cells under hypoxic conditions. Then, ELISA was used to detect the expression of HIF-1α and VEGF in the culture medium, and CCK8 was used to assess the proliferation of vascular endothelial cells.【Results】After transfection with miR-484 mimics, the proliferation capacity of SCG-7901 cells was significantly reduced, while the proliferation capacity of cells in the miR-484 inhibitor group was significantly increased. Compared to the miR-NC group, HIF-1α and VEGF mRNA and protein expression levels were downregulated in the miR-484 mimics group (all P<0.01), while the opposite results were observed in the miR-484 inhibitor group. Under hypoxic conditions, the levels of HIF-1α and VEGF in the culture medium of the miR-484 mimics group were much lower than those of the miR-NC group (both P<0.05), while the proliferation of vascular endothelial cells was higher (P<0.05). The results of the miR-484 inhibitor group were the opposite.【Conclusion】The miR-484 inhibits gastric cancer cell proliferation and tumor angiogenesis by downregulating the HIF-1α/VEGF pathway.

Key words： Stomach Neoplasms Neovascularization,Pathologic MicroRNAs Signal Transduction Vascular Endothelial Growth Factors

Received: 28 June 2024

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R735.2

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http://journal07.magtech.org.cn/yxlcyj/EN/10.3969/j.issn.1671-7171.2024.09.003 OR http://journal07.magtech.org.cn/yxlcyj/EN/Y2024/V41/I9/1289

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