Department of Biomedical Engineering, Lerner Research Institute, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH, 44195, USA.
Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH, USA.
Drug Deliv Transl Res. 2018 Oct;8(5):1289-1299. doi: 10.1007/s13346-018-0556-y.
Epigenetic modifications (e.g., DNA methylation or histone deacetylation) are commonly implicated in cancer chemoresistance. We previously showed that pretreating resistant MCF-7/ADR breast cancer cells with a demethylating agent (5-aza-2'-deoxycytidine (DAC)) or with an inhibitor of histone deacetylase (suberoylanilide hydroxamic acid (SAHA)) sensitized resistant cells to doxorubicin (DOX) treatment. However, even with increasing doses of DOX, a fraction of resistant cells remained nonresponsive to this pretreatment (~ 25% pretreated with DAC, ~ 45% with SAHA). We hypothesized that pretreating resistant cells with a combination of epigenetic drugs (DAC + SAHA) could more effectively overcome drug resistance. We postulated that delivery of epigenetic drugs encapsulated in biodegradable nanogels (NGs) would further enhance their efficacy. MCF-7/ADR cells were first treated with a single drug vs. a combination of epigenetic drugs, either as solutions or encapsulated in NGs, then subjected to DOX, either in solution or in NGs. Antiproliferative data showed that pretreatment with epigenetic drugs in NGs, then with DOX in NGs, was most effective in overcoming resistance; this treatment inhibited cell growth by > 90%, even at low doses of DOX. Cell cycle analysis showed that a major fraction of cells treated with a cocktail of epigenetic drugs + DOX, all in NG formulations, remained in the G2/M cell cycle arrest phase for a prolonged period. The mechanism of better efficacy of epigenetic drugs in NGs could be attributed to their sustained effect. A similar strategy could be developed for other cancer cells in which drug resistance is due to epigenetic modifications.
表观遗传修饰(例如 DNA 甲基化或组蛋白去乙酰化)通常与癌症化疗耐药有关。我们之前的研究表明,用去甲基化剂(5-氮杂-2'-脱氧胞苷(DAC))或组蛋白去乙酰化酶抑制剂(丁酸钠(SAHA))预处理耐药 MCF-7/ADR 乳腺癌细胞可使耐药细胞对阿霉素(DOX)治疗敏感。然而,即使增加 DOX 的剂量,仍有一部分耐药细胞对这种预处理无反应(25%用 DAC 预处理,45%用 SAHA 预处理)。我们假设用联合使用表观遗传药物(DAC+SAHA)预处理耐药细胞可以更有效地克服耐药性。我们推测,将表观遗传药物封装在可生物降解的纳米凝胶(NGs)中可以进一步提高其疗效。首先,将 MCF-7/ADR 细胞用单一药物或联合使用表观遗传药物处理,无论是溶液形式还是封装在 NGs 中,然后用 DOX 处理,无论是溶液形式还是封装在 NGs 中。抗增殖数据表明,用 NG 中封装的表观遗传药物预处理,然后用 NG 中 DOX 处理,是克服耐药性最有效的方法;这种治疗方法即使在低剂量 DOX 下,也能使细胞生长抑制超过 90%。细胞周期分析表明,用包含 DOX 的表观遗传药物鸡尾酒处理的细胞,大部分仍处于 NG 制剂中 G2/M 细胞周期阻滞期,持续时间较长。在 NG 中,表观遗传药物疗效更好的机制可能归因于其持续作用。对于其他由于表观遗传修饰而产生耐药性的癌细胞,也可以开发出类似的策略。