Research Papers:

This article has been corrected. Correction in: Oncotarget. 2020; 11:300-301.

Wogonin induces cell cycle arrest and erythroid differentiation in  imatinib-resistant K562 cells and primary CML cells

Hao Yang, Hui Hui, Qian Wang, Hui Li, Kai Zhao, Yuxin Zhou, Yu Zhu, Xiaotang Wang, Qidong You, Qinglong Guo _ and Na Lu

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Oncotarget. 2014; 5:8188-8201. https://doi.org/10.18632/oncotarget.2340

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Hao Yang1,*, Hui Hui1,*, Qian Wang1, Hui Li1, Kai Zhao1, Yuxin Zhou1, Yu Zhu3, Xiaotang Wang2, Qidong You1, Qinglong Guo1 and Na Lu1

1 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

2 Department of Chemistry and Biochemistry, Florida International University, Miami, FL, USA

3 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

* These authors contributed equally to this work


Qing-Long Guo, email:

Na Lu, email:

Keywords: wogonin; CML; GATA-1; differentiation; cell cycle

Received: May 15, 2014 Accepted: August 09, 2014 Published: August 10, 2014


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.

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