Yang Hao, Hui Hui, Wang Qian, Li Hui, Zhao Kai, Zhou Yuxin, Zhu Yu, Wang Xiaotang, You Qidong, Guo Qinglong, Lu Na
State Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Carcinogenesis and Intervention, Key Laboratory of Drug Quality Control and Pharmacovigilance, Ministry of Education, China Pharmaceutical University, 24 Tongjiaxiang, Nanjing, People's Republic of China.
Department of Hematology, The First Affiliated Hospital of Nanjing Medical University; Department of Hematology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, Jiangsu Province, People's Republic of China.
Oncotarget. 2014 Sep 30;5(18):8188-201. doi: 10.18632/oncotarget.2340.
Wogonin, a flavonoid derived from Scutellaria baicalensis Georgi, has been demonstrated to be highly effective in treating hematologic malignancies. In this study, we investigated the anticancer effects of wogonin on K562 cells, K562 imatinib-resistant cells, and primary patient-derived CML cells. Wogonin up-regulated transcription factor GATA-1 and enhanced binding between GATA-1 and FOG-1, thereby increasing expression of erythroid-differentiation genes. Wogonin also up-regulated the expression of p21 and induced cell cycle arrest. Studies employing benzidine staining and analyses of cell surface markers glycophorin A (GPA) and CD71 indicated that wogonin promoted differentiation of K562, imatinib-resistant K562, and primary patient-derived CML cells. Wogonin also enhanced binding between GATA-1 and MEK, resulting in inhibition of the growth of CML cells. Additionally, in vivo studies showed that wogonin decreased the number of CML cells and prolonged survival of NOD/SCID mice injected with K562 and imatinib-resistant K562 cells. These data suggested that wogonin induces cycle arrest and erythroid differentiation in vitro and inhibits proliferation in vivo.
汉黄芩素是一种从黄芩中提取的黄酮类化合物，已被证明在治疗血液系统恶性肿瘤方面具有高效性。在本研究中，我们调查了汉黄芩素对K562细胞、K562伊马替尼耐药细胞以及原发性患者来源的慢性粒细胞白血病（CML）细胞的抗癌作用。汉黄芩素上调转录因子GATA-1并增强GATA-1与FOG-1之间的结合，从而增加红系分化基因的表达。汉黄芩素还上调p21的表达并诱导细胞周期停滞。采用联苯胺染色以及对细胞表面标志物血型糖蛋白A（GPA）和CD71进行分析的研究表明，汉黄芩素促进K562细胞、伊马替尼耐药K562细胞以及原发性患者来源的CML细胞的分化。汉黄芩素还增强GATA-1与MEK之间的结合，从而抑制CML细胞的生长。此外，体内研究表明，汉黄芩素减少了CML细胞的数量，并延长了注射K562细胞和伊马替尼耐药K562细胞的NOD/SCID小鼠的生存期。这些数据表明汉黄芩素在体外诱导细胞周期停滞和红系分化，并在体内抑制增殖。
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