Lee Sang Hyuk, Nam Hyo Jung, Kang Hyun Jung, Samuels Tina L, Johnston Nikki, Lim Young Chang
Department of Otorhinolaryngology-Head and Neck Surgery, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea.
Department of Otorhinolaryngology-Head and Neck Surgery, Research Institute of Medical Science, Konkuk University School of Medicine, Seoul, Republic of Korea.
Oncol Rep. 2015 Oct;34(4):2065-71. doi: 10.3892/or.2015.4145. Epub 2015 Jul 23.
Emerging evidence suggests that cancer cells present profound epigenetic alterations in addition to featuring classic genetic mutations. Valproic acid (VPA), a histone deacetylase inhibitor, can potently inhibit tumor growth and induce differentiation. However, the effect and underlying mechanism of VPA on head and neck squamous cell carcinoma (HNSCC) cancer stem cells (CSCs) remain unclear. In the present study we investigated the effects of VPA on the characteristics of HNSCC CSCs in vitro and in vivo. As a result, VPA inhibited the self-renewal abilities of HNSCC CSCs during two serial passages and decreased the expression of stem cell markers, such as Oct4, Sox2 and CD44. VPA also potentiated the cytotoxic effect of cisplatin by suppressing the ABCC2 and ABCC6 transporters as well as by inducing caspase-mediated apoptosis. In addition, the combination of VPA and cisplatin attenuated tumor growth and induced apoptosis in a xenograft model. Our results suggest that VPA might be a potential therapeutic strategy in combination with conventional cisplatin for HNSCC patients by elimination of CSC traits.
新出现的证据表明,癌细胞除了具有经典的基因突变外,还存在深刻的表观遗传改变。丙戊酸(VPA)是一种组蛋白去乙酰化酶抑制剂,能有效抑制肿瘤生长并诱导分化。然而,VPA对头颈部鳞状细胞癌(HNSCC)癌症干细胞(CSCs)的作用及潜在机制仍不清楚。在本研究中,我们调查了VPA在体外和体内对HNSCC CSCs特性的影响。结果显示,VPA在连续两代传代过程中抑制了HNSCC CSCs的自我更新能力,并降低了干细胞标志物如Oct4、Sox2和CD44的表达。VPA还通过抑制ABCC2和ABCC6转运蛋白以及诱导半胱天冬酶介导的凋亡来增强顺铂的细胞毒性作用。此外,在异种移植模型中,VPA和顺铂联合使用可减缓肿瘤生长并诱导凋亡。我们的结果表明,通过消除CSC特性,VPA可能是一种与传统顺铂联合用于HNSCC患者的潜在治疗策略。