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Comp34 displays potent preclinical antitumor efficacy in triple-negative breast cancer via inhibition of NUDT3-AS4 a novel oncogenic long noncoding RNA

机译:Comp34通过抑制NUDT3-AS4通过NUDT3-AS4显示三重阴性乳腺癌中有效的临床前抗肿瘤疗效这是一种新型致癌的长度非致rna

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摘要

a Screening growth-inhibitory effects of 33 curcumin derivatives on MDA-MB-231 cells. b Chemical structure of Comp34. c IC50 values exhibited by Comp34 for cytotoxicity against various breast cancer cell lines and nontumorigenic breast epithelial cells. d Phosphorylation status of 34 kinases or transcription factors was assessed by the proteome profiler human phospho-kinase array. e Relative phosphorylation of spots was quantified by normalizing pixel density of the positive control to 100. f Western blotting (WB) analysis of the expression of AKT1, p-AKT, mTOR, p-p70S6K, p-S6, p-4EBP1 in the MDA-MB-231 cell line upon different concentrations of Comp34 treatment. g Reduction of AKT1 and mTOR mRNA expression in MDA-MB-231 cells treated with Comp34 analyzed by qRT-PCR (n = 3 replicates). *P < 0.05 versus control. h Dissociation of mammospheres after treatment with Comp34. The results represent the mean diameter of mammospheres ± SD, n = 6. i Comp34 reduced the stemness of MDA-MB-231 cells in a dose-dependent manner. Stem cell populations were analyzed by FACS using CD44 and CD24 antibodies. US unstained. The results represent the mean percentage of stem cell population ± SD, n = 6.
机译:33种姜黄素衍生物对MDA-MB-231细胞的筛选生长抑制作用。 B Comp34的化学结构。 COM50由Comp34表现出对各种乳腺癌细胞系和非致植物乳房上皮细胞的细胞毒性。 D 34激酶或转录因子的D磷酸化状态由蛋白质组分布器人磷酸激酶阵列评估。通过将阳性对照的像素密度标准化为100.FWesters的印迹(Wb)分析Akt1,P-Akt,MTOR,P-P70S6K,P-S6,P-4EBP1的表达式来定量斑点的相对磷酸化MDA-MB-231细胞系在不同浓度的Comp34处理。通过QRT-PCR分析用COMP34处理的MDA-MB-231细胞中的AKT1和MTOR mRNA表达的G(n = 3重复)。 * P <0.05与控制。 COMP34治疗后乳房层的H离解。结果代表静脉内±SD的平均直径,N = 6. I COMP34以剂量依赖性方式降低了MDA-MB-231细胞的茎。使用CD44和CD24抗体分析干细胞群。美国未染色。结果代表干细胞群±SD,n = 6的平均百分比。

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