木蝴蝶苷A通过调控MEK/ERK信号通路对肝癌细胞增殖侵袭和上皮间质转化的机制研究

doi:10.3969/j.issn.1006-6233.2023.03.01

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Abstract Objective: To investigate the mechanism of luteolin A on proliferation, invasion and epithelial mesenchymal transformation of hepatocellular carcinoma cells by regulating MEK/ERK signaling pathway. Methods: HepG2 cells were divided into control group, OAL group, OAM group, OAH group, PD98059 group and ML-099 group. MTT assay was used to detect cell proliferation; Transwell chamber method was used to detect the invasive ability of cells; Apoptosis was detected by flow cytometry; the expression of MEK.p-MEK, ERK.p-ERK and EMT related proteins were detected by Western blot. Results: The cell proliferation and invasion ability of OAL group, OAM group and OAH group (82.34 ± 2.43), (61.04 ± 1.61) and (32.44 ± 1.04) were significantly lower than those of the control group (110.42 ± 3.86), and the cell apoptosis rate in those group (6.81 ± 0.62), (11.74 ± 0.94) and (18.36 ± 1.05) were significantly higher than those of the control group (5.01 ± 0.53) (F_invasion=1068, F_apoptosis=323.1, P<0.001); the expression of E-cadherin protein (0.42 ± 0.04), (0.58 ± 0.05) and (0.97 ± 0.09) in the cells was higher than that in the control group (0.23 ± 0.03) (F=181.1, P<0.001); N-cadherin (0.63 ± 0.06), (0.51 ± 0.05), (0.38 ± 0.03), Vimentin (1.23 ± 0.11), (0.98 ± 0.09), (0.51 ± 0.05) and p-MEK/MEK (0.72 ± 0.07), (0.51 ± 0.05), (0.32 ± 0.03) and p-ERK/ERK (0.92 ± 0.09), (0.68 ± 0.06). The ratio (0.41 ± 0.04) was lower than that of the control group (FF_N-cadherin=39.04, FF_Vimentin=11.0, FF_p-MEK/ME=107.8, FF_p-ERK/ERK=82.68, P<0.001). The cell proliferation and invasion ability (30.86 ± 1.01) of PD98059 group was significantly lower than that of the control group (t=48.84, P<0.001), the cell apoptosis ability (17.95 ± 0.98) was significantly higher than that of the control group (t=28.45, P<0.001), the epithelial mesenchymal transformation protein E-cadherin protein (0.92 ± 0.09) was significantly higher than that of the control group (t=17.82, P<0.001), the epithelial mesenchymal transformation protein N-cadherin (0.37 ± 0.04) (t=9.585),vimentin protein (0.41 ± 0.04) (t=19.99) and p-MEK/MEK (0.30 ± 0.03) (t=16.78), p-ERK/ERK (0.39 ± 0.04) (t=14.65) were significantly lower than those in the control group (P<0.001). The cell proliferation and invasion ability (100.86 ± 2.68) of ML-099 group was significantly higher than that of OAH group (t=12.54, P<0.001), and the cell apoptosis ability (5.15 ± 0.86) was significantly lower than that of OAH group (t=23.84, P<0.001); compared with OAH group, E-cadherin protein (0.25 ± 0.03) was significantly decreased in ML-099 group (t=18.59, P<0.001), and N-cadherin protein (0.69 ± 0.07) (t=0.971, P<0.001), Vimentin protein (1.50 ± 0.12) (t=18.65, P<0.0001), p-MEK/MEK (0.94 ± 0.09) (t=16.01, P<0.001), p-ERK/ERK (1.05 ± 0.10) (t=2.367, P=0.0395) were significantly increased in ML-099 group. Conclusion: Luteolin A can inhibit the proliferation, invasion and epithelial mesenchymal transformation of liver cancer cells, and induce apoptosis of liver cancer cells. Its mechanism is related to inhibition of MEK/ERK signaling pathway.

Key words： Luteolin A MEK/ERK signal path Proliferation Attack Apoptosis Epithelial mesenchymal transformation

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http://www.hbyxzzs.cn/EN/10.3969/j.issn.1006-6233.2023.03.01 OR http://www.hbyxzzs.cn/EN/Y2023/V29/I3/353

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