当前位置: X-MOL 学术Toxicol. In Vitro › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
A tetraprenylated benzophenone 7-epiclusianone induces cell cycle arrest at G1/S transition by modulating critical regulators of cell cycle in breast cancer cell lines.
Toxicology in Vitro ( IF 3.2 ) Pub Date : 2020-07-04 , DOI: 10.1016/j.tiv.2020.104927
Simone da Silva Lamartine-Hanemann 1 , Guilherme Álvaro Ferreira-Silva 1 , Renato de Oliveira Horvath 1 , Roseli Soncini 1 , Ester Siqueira Caixeta 1 , Bianca Rocha-Sales 2 , Evandro Luís Niero 2 , Glaucia Maria Machado-Santelli 2 , Marcelo Henrique Dos Santos 3 , Jaqueline Carvalho de Oliveira 4 , Marta Miyazawa 5 , Marisa Ionta 6
Affiliation  

Breast cancer is a complex disease and encompassing different types of tumor. Although advances in understanding of the molecular bases of breast cancer biology, the therapeutic proposals available still are not effective. In this scenario, the present study aimed to evaluate the mechanisms associated to antitumor activity of 7-Epiclusianone (7-Epi), a tetraprenylated benzophenone, on luminal A (MCF-7) and claudin-low (Hs 578T) breast cancer cell lines. We found that 7-Epi efficiently inhibited cell proliferation and migration of these cells; however MCF-7 was slightly more responsive than Hs 578T. Cell cycle analysis showed accumulation of cells at G0/G1 phase with drastic reduction of S population in treated cultures. This effect was associated to downregulation of CDKN1A (p21) and cyclin E in both cell lines. In addition, 7-Epi reduced cyclin D1 and p-ERK expression levels in MCF-7 cell line. Cytotoxic effect of 7-Epi on breast cancer cell lines was associated to its ability to increase BAX/BCL-2 ratio. In conclusion, our findings showed that 7-Epi is a promising antitumor agent against breast cancer by modulating critical regulators of the cell cycle and apoptosis.



中文翻译:

通过调节乳腺癌细胞系中细胞周期的关键调控因子,四戊烯基化的二苯甲酮7-表氯酮可以诱导G1 / S过渡时的细胞周期停滞。

乳腺癌是一种复杂的疾病,涵盖了不同类型的肿瘤。尽管在了解乳腺癌生物学的分子基础方面取得了进步,但是可用的治疗方案仍然无效。在这种情况下,本研究旨在评估与管腔A(MCF-7)和低claudin-low(Hs 578T)乳腺癌细胞系上的7-Epiclusianone(7-Epi),四prenynylated苯甲酮的抗肿瘤活性相关的机制。我们发现7-Epi有效抑制了这些细胞的细胞增殖和迁移。然而,MCF-7的反应能力比Hs 578T略高。细胞周期分析显示,在处理的培养物中,G0 / G1期细胞蓄积,S种群急剧减少。这种作用与CDKN1A的下调有关(p21)和两种细胞系中的细胞周期蛋白E。此外,7-Epi降低了MCF-7细胞系中的细胞周期蛋白D1和p-ERK表达水平。7-Epi对乳腺癌细胞系的细胞毒作用与其增加BAX / BCL-2比的能力有关。总之,我们的研究结果表明7-Epi通过调节细胞周期和细胞凋亡的关键调节剂,是一种有前景的抗乳腺癌抗肿瘤药。

更新日期:2020-07-13
down
wechat
bug