背景:研究表明花青素对乳腺癌癌变的化学预防作用。本系统评价和荟萃分析旨在评估花色苷对体外培养的三阴性乳腺癌细胞(TNBC)的影响。
方法:我们搜索了所有评估迁移机制的相关研究,入侵,Akt/mTOR和MAPK途径,和细胞凋亡,使用PubMed和Scopus。使用平均值和标准偏差,并应用了随机效应模型,置信区间为95%。使用Chi2检验和I2统计量评估研究之间的统计异质性。使用RevMan软件(版本5.4)进行所有分析。
结果:11项研究纳入系统综述,10项纳入荟萃分析,其中研究了富含花青素的提取物或花青素-3-O-葡萄糖苷(C-3-O-G)对MDA-MB-231和MDA-MB-453细胞的作用。
结论:花青素处理后,TNBC细胞的侵袭(平均差:-98.64;95%CI:-153.98,-43.3;p<0.00001)和迁移(平均差:-90.13;95%CI:-130.57,-49.68;p<0.00001)显着降低。花青素还下调Akt(平均差:-0.63;95%CI:-0.70,-0.57;p=0.00001)和mTOR(平均差:-0.93;95%CI:-1.58,-0.29;p=0.005),而JNK(平均差异:-0.06;95%CI:-1.21,1.09;p=0.92)和p38(平均差异:0.05;95%CI:-1.32,1.41;p=0.95)未被调节。裂解的caspase-3也增加(平均差:1.13;95%CI:0.11,2.16;p=0.03),calvedcaspase-8(平均差:1.64;95%CI:0.05,3.22;p=0.04),和切割的PARP(平均差:0.93;95%CI:0.54,1.32)。尽管对照组和花色苷组之间的凋亡率差异不显著(平均差异:3.63;95%CI:-2.88,10.14;p=0.27),亚组之间的分析表明,花色苷更有利于诱导整体细胞凋亡(p=0.00001)。
结论:结果表明,花青素在对抗TNBC方面有希望,但是它们的影响不应该一概而论。此外,应进行进一步的初步研究,以便得出更准确的结论。
BACKGROUND: Studies have suggested the chemopreventive effects of anthocyanins on breast cancer carcinogenesis. This systematic review and meta-analysis aimed to evaluate the effect of anthocyanins on triple-negative breast cancer cells (TNBC) cultured in vitro.
METHODS: We searched for all relevant studies that evaluated the mechanisms of migration, invasion, Akt/mTOR and MAPK pathways, and apoptosis, using PubMed and Scopus. Means and standard deviation were used, and a randomized effects model was applied, with a confidence interval of 95%. Statistical heterogeneity between studies was assessed using the Chi2 test and I2 statistics. All analyses were performed using RevMan software (version 5.4).
RESULTS: Eleven studies were included in the systematic review and ten in the meta-analysis, where the roles of anthocyanin-enriched extract or cyanidin-3-O-glucoside (C-3-O-G) on MDA-MB-231 and MDA-MB-453 cells were investigated.
CONCLUSIONS: There was a significant reduction in invasion (mean difference: -98.64; 95% CI: -153.98, -43.3; p ˂ 0.00001) and migration (mean difference: -90.13; 95% CI: -130.57, -49.68; p ˂ 0.00001) in TNBC cells after anthocyanins treatment. Anthocyanins also downregulated Akt (mean difference: -0.63; 95% CI: -0.70, -0.57; p ˂ 0.00001) and mTOR (mean difference: -0.93; 95% CI: -1.58, -0.29; p = 0.005), while JNK (mean difference: -0.06; 95% CI: -1.21, 1.09; p = 0.92) and p38 (mean difference: 0.05; 95% CI: -1.32, 1.41; p = 0.95) were not modulated. There was also an increase in cleaved caspase-3 (mean difference: 1.13; 95% CI: 0.11, 2.16; p = 0.03), cleaved caspase-8 (mean difference: 1.64; 95% CI: 0.05, 3.22; p = 0.04), and cleaved PARP (mean difference: 0.93; 95% CI: 0.54, 1.32). Although the difference between control and anthocyanin groups was not significant regarding apoptosis rate (mean difference: 3.63; 95% CI: -2.88, 10.14; p = 0.27), the analysis between subgroups showed that anthocyanins are more favorable in inducing overall apoptosis (p ˂ 0.00001).
CONCLUSIONS: The results show that anthocyanins hold promise in fighting against TNBC, but their effects should not be generalized. In addition, further primary studies should be conducted so that more accurate conclusions can be drawn.