Park Ki Cheong, Kim Seok-Mo, Jeon Jeong Yong, Kim Bup-Woo, Kim Hyeung Kyoo, Chang Ho Jin, Lee Yong Sang, Kim Soo Young, Choi Seung Hoon, Park Cheong Soo, Chang Hang-Seok
Thyroid Cancer Center, Gangnam Severance Hospital, Department of Surgery, Yonsei University College of Medicine, Seoul 120-752, Republic of Korea; Gangnam Severance Hospital, Department of Surgery, Yonsei University College of Medicine, Seoul 120-752, Republic of Korea.
Department of Nuclear Medicine, Yonsei College of Medicine, Seoul 120-752, Republic of Korea.
Neoplasia. 2017 Mar;19(3):145-153. doi: 10.1016/j.neo.2016.12.005. Epub 2017 Jan 28.
Anaplastic thyroid carcinoma (ATC) although rare is the most deadly form of thyroid cancer. The fatality rate for ATC is high-pitched, the survival rate at 1 year after diagnosis is <20%. Control of ATC is severely hard and widespread with unpredictability. We Previous proved that histone gene reviser and epigenetic changes role significant parts in papillary and anaplastic thyroid cancer tumorigenesis. Herein, the goal of this study was to investigate the anti-tumor activities of a HDAC inhibitor, HNHA alone and in combination with sorafenib in ATC cells in vitro and in vivo and to explore its effects on apoptotic cell death pathways. Three ATC cell lines were exposed to sorafenib in the presence or absence of HNHA, and cell viability was determined by MTT assay. Effects of combined treatment on cell cycle and intracellular signaling pathways were assessed by flow cytometry and western blot analysis. The ATC cell lines xenograft model was used to examine the anti-tumor activity in vivo. Our data showed that HNHA and sorafenib synergistically decreased cell viability in ATC cells, and also significantly increased apoptotic cell death in these cells, as proved by the cleavage of caspase-3 and DNA fragmentation. HNHA and sorafenib combination was reduced anti-apoptotic factor in ATC. Thus, combination therapy with HNHA and sorafenib significantly decreased vessel density, and most significantly reduced tumor volume and increased survival in ATC xenografts. These results propose that HNHA in combination with sorafenib has significant anti-cancer activity in preclinical models, potentially suggesting a new clinical approach for patients of advanced thyroid cancer type.
间变性甲状腺癌(ATC)虽然罕见,但却是甲状腺癌最致命的形式。ATC的死亡率很高,诊断后1年的生存率<20%。ATC的控制非常困难且普遍存在不可预测性。我们之前证明组蛋白基因修饰和表观遗传变化在乳头状和间变性甲状腺癌的肿瘤发生中起重要作用。在此,本研究的目的是研究一种组蛋白去乙酰化酶(HDAC)抑制剂HNHA单独及与索拉非尼联合在体外和体内对ATC细胞的抗肿瘤活性,并探讨其对凋亡细胞死亡途径的影响。将三种ATC细胞系在有或无HNHA的情况下暴露于索拉非尼,通过MTT法测定细胞活力。通过流式细胞术和蛋白质印迹分析评估联合治疗对细胞周期和细胞内信号通路的影响。使用ATC细胞系异种移植模型来检测体内抗肿瘤活性。我们的数据表明,HNHA和索拉非尼协同降低了ATC细胞的活力,并且还显著增加了这些细胞中的凋亡细胞死亡,这通过半胱天冬酶-3的裂解和DNA片段化得到证实。HNHA和索拉非尼联合降低了ATC中的抗凋亡因子。因此,HNHA与索拉非尼联合治疗显著降低了血管密度,最显著地减小了肿瘤体积并提高了ATC异种移植的生存率。这些结果表明,HNHA与索拉非尼联合在临床前模型中具有显著的抗癌活性,这可能为晚期甲状腺癌患者提出一种新的临床治疗方法。