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Sinomenine restrains breast cancer cells proliferation, migration and invasion via modulation of miR-29/PDCD-4 axis

机译:青藤碱通过调节miR-29 / PDCD-4轴来抑制乳腺癌细胞的增殖,迁移和侵袭

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Sinomenine (Sino) is diffusely applied in heal rheumatoid arthritis and neuralgia. Howbeit, the activities of Sino in breast cancer cells remain confused. The research attempted to probe the anti-tumor function of Sino in breast cancer cells and divulge the feasible molecular mechanism. Sion at the 1–16?μM concentrations was exploited for the exposure of MDA-MB-231 or MCF7 cells, and cell growth, migration, invasion, cell cycle-relevant and apoptosis-correlative factors were estimated. Micro RNA (miR)-29 expression was evaluated via enforcing qRT-PCR, and the actions of miR-29 in MDA-MB-231 cells growth, migration and invasion were appraised after the overexpressed or suppressed vectors transfection. The functions of PDCD-4 in JNK and MEK/ERK pathways were estimated by employing western blot. We found that, Sino exposure impeded cell proliferation, provoked cell apoptosis and barricaded cell migration and invasion in MDA-MB-231 and MCF7 cells. Enhancement of miR-29 was observed in Sino-managed cells, and miR-29 overexpression further potentiated the activities of Sino in MDA-MB-231 cells. Additionally, Sino remarkably enhanced PCDC-4 expression via adjusting miR-29 in MDA-MB-231 cells. Beyond that, overexpressed PCDC-4 obstructed JNK and MEK/ERK pathways in MDA-MB-231 cells. Taken together, the explorations unveiled that Sino restrained MDA-MB-231 cells proliferation, migration, invasion, and provoked apoptosis through modulation of miR-29/PDCD-4 axis. Highlight Sino inhibits MDA-MB-231 and MCF7 cells proliferation and provokes apoptosis; Sino restrains MDA-MB-231 and MCF7 cells migration and invasion; Sino ascends miR-29 expression in MDA-MB-231 and MCF7 cells; Sino adjusts cell growth, migration and invasion via modulating miR-29; Sino up-regulates PDCD-4 expression through mediating miR-29; PDCD-4 obstructs JNK and MEK/ERK pathways in MDA-MB-231 cells.
机译:青藤碱(Sinomenine)广泛用于治疗类风湿关节炎和神经痛。然而,Sin在乳腺癌细胞中的活性仍然令人困惑。该研究试图探讨Sin在乳腺癌细胞中的抗肿瘤功能,并揭示可行的分子机制。利用浓度为1–16?M的Sion暴露MDA-MB-231或MCF7细胞,并评估了细胞生长,迁移,侵袭,细胞周期相关因子和凋亡相关因子。通过执行qRT-PCR评估微小RNA(miR)-29的表达,并在过度表达或抑制载体转染后评估miR-29在MDA-MB-231细胞生长,迁移和侵袭中的作用。 PDCD-4在JNK和MEK / ERK途径中的功能通过采用蛋白质印迹法进行评估。我们发现,中毒暴露会阻碍MDA-MB-231和MCF7细胞的增殖,引发细胞凋亡以及阻碍细胞迁移和侵袭。在Sino管理的细胞中观察到miR-29的增强,而miR-29的过表达进一步增强了MDA-MB-231细胞中Sino的活性。此外,Sino通过调节MDA-MB-231细胞中的miR-29显着增强了PCDC-4的表达。除此之外,过度表达的PCDC-4阻碍了MDA-MB-231细胞中的JNK和MEK / ERK途径。综上所述,这些探索揭示了Sino通过调节miR-29 / PDCD-4轴来抑制MDA-MB-231细胞的增殖,迁移,侵袭和引发细胞凋亡。突出显示Sino抑制MDA-MB-231和MCF7细胞增殖并引起细胞凋亡。 Sino抑制MDA-MB-231和MCF7细胞迁移和侵袭。赛诺提高了MDA-MB-231和MCF7细胞中miR-29的表达; Sino通过调节miR-29来调节细胞的生长,迁移和侵袭; Sino通过介导miR-29上调PDCD-4表达; PDCD-4阻碍了MDA-MB-231细胞中的JNK和MEK / ERK途径。

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