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葡萄多酚抑制 Akt/雷帕霉素靶蛋白信号通路并增强吉非替尼在乳腺癌中的作用。

Grape polyphenols inhibit Akt/mammalian target of rapamycin signaling and potentiate the effects of gefitinib in breast cancer.

机构信息

Department of Biochemistry, School of Medicine, University of Puerto Rico, Medical Sciences Campus, San Juan, Puerto Rico.

出版信息

Nutr Cancer. 2012;64(7):1058-69. doi: 10.1080/01635581.2012.716898.

Abstract

We recently reported that a combination of dietary grape polyphenols resveratrol, quercetin, and catechin (RQC), at low concentrations, was effective at inhibiting metastatic cancer progression. Herein, we investigate the molecular mechanisms of RQC in breast cancer and explore the potential of RQC as a potentiation agent for the epidermal growth factor receptor (EGFR) therapeutic gefitinib. Our in vitro experiments showed RQC induced apoptosis in gefitinib-resistant breast cancer cells via regulation of a myriad of proapoptotic proteins. Because the Akt/mammalian target of rapamycin (mTOR) signaling pathway is often elevated during development of anti-EGFR therapy resistance, the effect of RQC on the mTOR upstream effector Akt and the negative regulator AMP kinase (AMPK) was investigated. RQC was found to reduce Akt activity, induce the activation of AMPK, and inhibit mTOR signaling in breast cancer cells. Combined RQC and gefitinib decreased gefitinib resistant breast cancer cell viability to a greater extent than RQC or gefitinib alone. Moreover, RQC inhibited Akt and mTOR and activated AMPK even in the presence of gefitinib. Our in vivo experiments showed combined RQC and gefitinib was more effective than the individual treatments at inhibiting mammary tumor growth and metastasis in nude mice. Therefore, RQC treatment inhibits breast cancer progression and may potentiate anti-EGFR therapy by inhibition of Akt/mTOR signaling.

摘要

我们最近报道,低浓度的膳食葡萄多酚(白藜芦醇、槲皮素和儿茶素)组合(RQC)可有效抑制转移性癌症的进展。在此,我们研究了 RQC 在乳腺癌中的分子机制,并探讨了 RQC 作为表皮生长因子受体(EGFR)治疗药物吉非替尼增效剂的潜力。我们的体外实验表明,RQC 通过调节多种促凋亡蛋白诱导吉非替尼耐药乳腺癌细胞凋亡。因为在抗 EGFR 治疗耐药性的发展过程中,Akt/哺乳动物雷帕霉素靶蛋白(mTOR)信号通路通常升高,所以研究了 RQC 对 mTOR 上游效应物 Akt 和负调节剂 AMP 激酶(AMPK)的作用。结果发现,RQC 降低 Akt 活性,诱导 AMPK 激活,并抑制乳腺癌细胞中的 mTOR 信号。与 RQC 或吉非替尼单独治疗相比,RQC 和吉非替尼联合使用可更大程度地降低吉非替尼耐药乳腺癌细胞的活力。此外,即使存在吉非替尼,RQC 也能抑制 Akt 和 mTOR 并激活 AMPK。我们的体内实验表明,RQC 和吉非替尼联合治疗比单独治疗更能有效抑制裸鼠乳腺肿瘤生长和转移。因此,RQC 治疗可抑制乳腺癌进展,并通过抑制 Akt/mTOR 信号增强抗 EGFR 治疗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ccd7/4286176/eb3c3412d76f/nihms-425339-f0001.jpg

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