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首页> 外文期刊>Cellular Physiology and Biochemistry >Berberine Suppresses TPA-Induced Fibronectin Expression through the Inhibition of VEGF Secretion in Breast Cancer Cells
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Berberine Suppresses TPA-Induced Fibronectin Expression through the Inhibition of VEGF Secretion in Breast Cancer Cells

机译：小Ber碱通过抑制乳腺癌细胞中的VEGF分泌抑制TPA诱导的纤连蛋白表达。

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Background/Aims: Berberine (BBR) is an isoquinoline alkaloid and is beneficial for the anticancer effect on a variety of human tumor cells. However, BBR's anti-angiogenesis property and its clinical potential as an inhibitor of tumor angiogenesis in breast cancer cells have not been fully elucidated. Here, we investigated the effect of BBR on TPA-induced VEGF and fibronectin (FN) as well as VEGF-induced FN in breast cancer cells. Methods: The secretion of VEGF protein was detected by ELISA. Fibronectin mRNA and protein expression was analyzed by Real-Time PCR and western blotting, respectively. The overexpressions of CA-MEK, and CA-Akt were examined by adenovirus system. Results: Our results showed that TPA, a tumor promoter, significantly increased the level of VEGF and FN expression in both MCF7 and T47D breast cancer cells. On the other hand, TPA-induced VEGF and FN expression was suppressed by LY294002, a PI-3K inhibitor. In contrast, the level of FN expression also significantly increased by constitutively active (CA)-AKT overexpression. We also found that TPA-induced VEGF and FN expression was decreased by BBR treatment. Finally, our results showed that VEGF augmented the expression of FN whereas VEGF-induced FN expression was decreased by BBR treatment. Conclusion: Taken together, we suggest that BBR may suppress TPA-induced VEGF and FN as well as VEGF-induced FN through the inhibition of the PI-3K/AKT pathway in breast cancer cells. Therefore, we suggest that BBR may be used as a candidate drug for the inhibition of angiogenesis of human breast cancer.
机译：背景/目的：小ber碱（BBR）是一种异喹啉生物碱，对多种人类肿瘤细胞具有抗癌作用。然而，尚未充分阐明BBR的抗血管生成特性及其作为乳腺癌细胞中肿瘤血管生成抑制剂的临床潜力。在这里，我们研究了乳腺癌细胞中BBR对TPA诱导的VEGF和纤连蛋白（FN）以及VEGF诱导的FN的影响。方法：采用ELISA法检测VEGF蛋白的分泌。纤连蛋白的mRNA和蛋白表达分别通过实时荧光定量PCR和蛋白质印迹分析。通过腺病毒系统检查CA-MEK和CA-Akt的过表达。结果：我们的结果表明，肿瘤启动子TPA显着增加了MCF7和T47D乳腺癌细胞中VEGF和FN的表达水平。另一方面，TPA诱导的VEGF和FN表达被PI-3K抑制剂LY294002抑制。相反，通过组成型活性（CA）-AKT的过表达，FN表达的水平也显着增加。我们还发现BBR治疗可降低TPA诱导的VEGF和FN表达。最后，我们的结果表明，通过BBR处理，VEGF增强了FN的表达，而VEGF诱导的FN表达却降低了。结论：综上所述，我们认为BBR可能通过抑制乳腺癌细胞中的PI-3K / AKT途径来抑制TPA诱导的VEGF和FN以及VEGF诱导的FN。因此，我们建议将BBR用作抑制人乳腺癌血管生成的候选药物。

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