This study assessed dark sweet cherry (DSC) phenolics as chemopreventive/chemotherapeutics against aggressive breast cancer subtypes.

DSC phenolics in whole extract (WE) and fractions enriched in phenolic acids (F1), flavonols (F3) and proanthocyanidins (F4) inhibited breast cancer cell growth with potency MDA-MB-453 > MDA-MB-231 ∼ BT-474, without toxicity to MCF-10A normal breast cells, except F3 that inhibited BT-474 and MCF-10A cells with similar toxicity. DSC anthocyanins (F2) inhibited breast cancer cell lines with similar potencies without toxicity to MCF-10A cells.

Mechanisms for WE, F2 and F4 breast anticancer activity may be mediated by reduction of oxidative stress, Akt/mTOR, p38, and survivin regulation, suggesting antiproliferative and apoptotic mechanisms. F2 significantly downregulated mRNA levels of invasive/metastatic biomarkers Sp1, Sp4, and VCAM-1, and Sp1 protein suggesting an enhanced chemopreventive/chemotherapeutic potential of DSC anthocyanins. Further studies are needed to elucidate underlying mechanisms of DSC phenolics as natural breast cancer chemopreventive compounds.

这项研究评估了深色甜樱桃（DSC）酚类药物作为针对侵袭性乳腺癌亚型的化学预防/化学疗法。

全提取物（WE）中的DSC酚类化合物以及富含酚酸（F1），黄酮醇（F3）和原花色素（F4）的馏分可有效抑制乳腺癌细胞的生长，MDA-MB-453> MDA-MB-231〜BT-474对MCF-10A正常乳腺细胞无毒性，但F3抑制BT-474和MCF-10A细胞毒性相似。DSC花色苷（F2）抑制乳腺癌细胞系具有相似的效力，而对MCF-10A细胞无毒性。

WE，F2和F4乳腺癌抗癌活性的机制可能是由氧化应激的降低，Akt / mTOR，p38和survivin调节介导的，提示了抗增殖和凋亡机制。F2显着下调了侵袭性/转移性生物标志物Sp1，Sp4和VCAM-1和Sp1蛋白的mRNA水平，表明DSC花青素具有更高的化学预防/化学治疗潜力。需要进一步研究阐明DSC酚类化合物作为天然乳腺癌化学预防化合物的潜在机制。