Chiaradonna Ferdinando, Barozzi Iros, Miccolo Claudia, Bucci Gabriele, Palorini Roberta, Fornasari Lorenzo, Botrugno Oronza A, Pruneri Giancarlo, Masullo Michele, Passafaro Alfonso, Galimberti Viviana E, Fantin Valeria R, Richon Victoria M, Pece Salvatore, Viale Giuseppe, Di Fiore Pier Paolo, Draetta Giulio, Pelicci Pier Giuseppe, Minucci Saverio, Chiocca Susanna
1 Department of Biotechnology and Biosciences, University of Milano-Bicocca , Milan, Italy .
2 SYSBIO Centre of Systems Biology , Milan, Italy .
Antioxid Redox Signal. 2015 Jul 1;23(1):15-29. doi: 10.1089/ars.2014.6189. Epub 2015 May 27.
Vorinostat (suberoylanilide hydroxamic acid; SAHA) is a histone deacetylase inhibitor (HDACi) approved in the clinics for the treatment of T-cell lymphoma and with the potential to be effective also in breast cancer. We investigated the responsiveness to SAHA in human breast primary tumors and cancer cell lines.
We observed a differential response to drug treatment in both human breast primary tumors and cancer cell lines. Gene expression analysis of the breast cancer cell lines revealed that genes involved in cell adhesion and redox pathways, especially glutathione metabolism, were differentially expressed in the cell lines resistant to SAHA compared with the sensitive ones, indicating their possible association with drug resistance mechanisms. Notably, such an association was also observed in breast primary tumors. Indeed, addition of buthionine sulfoximine (BSO), a compound capable of depleting cellular glutathione, significantly enhanced the cytotoxicity of SAHA in both breast cancer cell lines and primary breast tumors.
We identify and validate transcriptional differences in genes involved in redox pathways, which include potential predictive markers of sensitivity to SAHA.
In breast cancer, it could be relevant to evaluate the expression of antioxidant genes that may favor tumor resistance as a factor to consider for potential clinical application and treatment with epigenetic drugs (HDACis).
伏立诺他(辛二酰苯胺异羟肟酸;SAHA)是一种组蛋白去乙酰化酶抑制剂(HDACi),已在临床上获批用于治疗T细胞淋巴瘤,并且可能对乳腺癌也有效。我们研究了人乳腺原发性肿瘤和癌细胞系对SAHA的反应性。
我们观察到在人乳腺原发性肿瘤和癌细胞系中对药物治疗存在差异反应。对乳腺癌细胞系的基因表达分析表明,与细胞黏附及氧化还原途径相关的基因,尤其是谷胱甘肽代谢相关基因,在对SAHA耐药的细胞系中与敏感细胞系相比存在差异表达,这表明它们可能与耐药机制有关。值得注意的是,在乳腺原发性肿瘤中也观察到了这种关联。实际上,添加丁硫氨酸亚砜胺(BSO),一种能够消耗细胞内谷胱甘肽的化合物,显著增强了SAHA在乳腺癌细胞系和原发性乳腺肿瘤中的细胞毒性。
我们鉴定并验证了氧化还原途径相关基因的转录差异,其中包括对SAHA敏感性的潜在预测标志物。
在乳腺癌中,评估可能有利于肿瘤耐药的抗氧化基因的表达,作为潜在临床应用和表观遗传药物(HDACi)治疗时需要考虑的一个因素,可能具有重要意义。