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Xiantao First People's Hospital.
Cell Mol Biol (Noisy-le-grand). 2022 Feb 28;68(2):132-137. doi: 10.14715/cmb/2022.68.2.19.
The analyze the effect of miR-138 on the proliferation and apoptosis of breast cancer cells through the NF-κB/VEGF signaling pathway is the Objective of this experiment. For this aim, the endometrial stem breast cancer cell line MCF-7 was cultured in vitro, and the overexpression mimic miR-138 mimics and the inhibitor anti-miR-138 were transfected into the endometrial stem breast cancer cell line MCF-7, which was set to overexpress miR-138 group and interfere with miR-138, and set up negative control of overexpression and negative control of inhibitor. Observe the cell proliferation and apoptosis ability of each group, and the changes in tumor necrosis factor-α (TNF-α), interleukin 1β, 6, 18 (IL-1β, IL-6, IL-18) levels, and compare the Bax of each group, NF-κB, VEGF protein expression level. Results showed that the proliferation ability of the miR-138 overexpression group was significantly lower than that of the miR-138 overexpression control group (P<0.05); the proliferation ability of the miR-138 interference group was significantly higher than that of the miR-138 interference control group (P<0.05). The apoptosis rate, caspase-3 and caspase-9 expression levels of the miR-138 overexpression group were significantly higher than those of the miR-138 overexpression control group (P<0.05); the apoptosis rate, caspase-3 and caspase-9 expression levels of the miR-138 interference group were significantly lower than those of the miR-138 interference control group (P<0.05). The expression levels of IL-1 β, IL-6, IL-18 and TNF - α in the miR-138 overexpression group were significantly lower than those in the miR-138 overexpression control group (P < 0.05). The protein expression levels of Bax, NF-κB and VEGF in the miR-138 overexpression group were significantly lower than those in the miR-138 overexpression control group (P < 0.05); the protein expression levels of Bax, NF-κB and VEGF in the miR-138 interference group were significantly higher than those in the miR-138 interference control group (P <0.05). The proliferation ability of the miR-138 overexpression group was significantly lower than that of the miR-138 overexpression control group (P < 0.05); the proliferation ability of the miR-138 + NF-κB overexpression group was significantly higher than that of the miR-138 overexpression group (P<0.05). The apoptosis rate of the miR-138 + NF-κB overexpression group was significantly lower than that of the miR-138 overexpression group (P < 0.05). Then MiR-138 can significantly inhibit the proliferation of breast cancer cells, promote apoptosis, and regulate the expression of inflammatory factors in the cells. It is speculated that the related mechanism may be related to the negative regulation of the NF-κB/VEGF signaling pathway.
本实验旨在通过 NF-κB/VEGF 信号通路分析 miR-138 对乳腺癌细胞增殖和凋亡的影响。为此，将子宫内膜干细胞乳腺癌 MCF-7 细胞系在体外培养，并将过表达模拟物 miR-138 模拟物和抑制剂抗 miR-138 转染到子宫内膜干细胞乳腺癌 MCF-7 细胞系中，将其设定为过表达 miR-138 组和干扰 miR-138 组，并设置过表达阴性对照和抑制剂阴性对照。观察各组细胞的增殖和凋亡能力，以及肿瘤坏死因子-α（TNF-α）、白细胞介素 1β、6、18（IL-1β、IL-6、IL-18）水平的变化，并比较各组 Bax、NF-κB、VEGF 蛋白表达水平。结果表明，miR-138 过表达组的增殖能力明显低于 miR-138 过表达对照组（P<0.05）；miR-138 干扰组的增殖能力明显高于 miR-138 干扰对照组（P<0.05）。miR-138 过表达组的凋亡率、caspase-3 和 caspase-9 表达水平明显高于 miR-138 过表达对照组（P<0.05）；miR-138 干扰组的凋亡率、caspase-3 和 caspase-9 表达水平明显低于 miR-138 干扰对照组（P<0.05）。miR-138 过表达组的 IL-1β、IL-6、IL-18 和 TNF-α表达水平明显低于 miR-138 过表达对照组（P<0.05）。miR-138 过表达组 Bax、NF-κB 和 VEGF 蛋白表达水平明显低于 miR-138 过表达对照组（P<0.05）；miR-138 干扰组 Bax、NF-κB 和 VEGF 蛋白表达水平明显高于 miR-138 干扰对照组（P<0.05）。miR-138 过表达组的增殖能力明显低于 miR-138 过表达对照组（P<0.05）；miR-138+NF-κB 过表达组的增殖能力明显高于 miR-138 过表达组（P<0.05）。miR-138+NF-κB 过表达组的凋亡率明显低于 miR-138 过表达组（P<0.05）。因此，miR-138 可显著抑制乳腺癌细胞的增殖，促进细胞凋亡，并调节细胞内炎症因子的表达。推测其相关机制可能与负调控 NF-κB/VEGF 信号通路有关。
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