【佳学基因检测】Aurora 激酶 A 和 Bcl-xL 抑制抑制三阴性乳腺癌的转移
肿瘤基因检测多少钱一次—目标
小组讨论《肿瘤致病基因突变位点的性质及影响分析》《Int J Mol Sci》在. 2022 Sep 2;23(17):10053.发表了一篇题目为《Aurora 激酶 A 和 Bcl-xL 抑制抑制三阴性乳腺癌的转移》肿瘤靶向药物治疗基因检测临床研究文章。该研究由Natascha Skov, Carla L Alves, Sidse Ehmsen, Henrik J Ditzel 等完成。促进了肿瘤的精准治疗与个性化用药的发展,进一步强调了基因信息检测与分析的重要性。
肿瘤靶向药物及精准治疗临床研究内容关键词:
奥卡, BCL2L1, alisertib,基底样乳腺癌,上皮-间质转化
肿瘤靶向治疗基因检测临床应用结果
三阴性乳腺癌 (TNBC) 是一种异质性疾病,占所有乳腺癌病例的 10-15%。在 TNBC 中,基底 B 的治疗由于其高侵袭性潜力而最具挑战性,因此迫切需要抑制该亚组转移形成的治疗。然而,TNBC 转移能力的潜在机制仍不清楚。在本研究中,我们研究了 Aurora A 和 Bcl-xL 在调节基底 B 细胞侵袭中的作用。我们发现基底 B 细胞中的基因扩增和蛋白质表达升高,与基底 A 细胞相比,其在体外也显示出增加的侵袭性。与基础 B 细胞系中未处理的细胞相比,使用 alisertib 和 siRNA 介导的 BCL2L1 敲低对 Aurora A 的化学抑制减少了入侵细胞的数量。分析 TNBC 中 AURKA 和 BCL2L1 表达与患者生存率之间的相关性显示,原发性乳腺癌患者的无复发生存期(n = 534,p = 0.012)和无远处转移生存期(n = 424,p = 0.017)显着降低肿瘤表现出 AURKA 和 BCL2L1 的高组合表达。总之,我们的研究结果表明,高水平的 Aurora A 和 Bcl-xL 促进转移,抑制这些蛋白质可能会抑制转移并提高基础 B TNBC 患者的存活率。 BCL2L1; alisertib;基底样乳腺癌;上皮-间质转化。
肿瘤发生与复发转移国际数据库描述:
Triple-negative breast cancer (TNBC) is a heterogeneous disease that accounts for 10-15% of all breast cancer cases. Within TNBC, the treatment of basal B is the most challenging due to its highly invasive potential, and thus treatments to suppress metastasis formation in this subgroup are urgently needed. However, the mechanisms underlying the metastatic ability of TNBC remain unclear. In the present study, we investigated the role of Aurora A and Bcl-xL in regulating basal B cell invasion. We found gene amplification and elevated protein expression in the basal B cells, which also showed increased invasiveness in vitro, compared to basal A cells. Chemical inhibition of Aurora A with alisertib and siRNA-mediated knockdown of BCL2L1 decreased the number of invading cells compared to non-treated cells in basal B cell lines. The analysis of the correlation between AURKA and BCL2L1 expression in TNBC and patient survival revealed significantly decreased relapse-free survival (n = 534, p = 0.012) and distant metastasis-free survival (n = 424, p = 0.017) in patients with primary tumors exhibiting a high combined expression of AURKA and BCL2L1. Together, our findings suggest that high levels of Aurora A and Bcl-xL promote metastasis, and inhibition of these proteins may suppress metastasis and improve patient survival in basal B TNBC.Keywords: AURKA; BCL2L1; alisertib; basal-like breast cancer; epithelial–mesenchymal transition.
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