Abstract
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.
Highlights
The K562 cells were derived from a patient suffering from chronic myelogenous leukemia (CML) blast crisis phase and used as the cell line for the research of erythroid differentiation[1, 2]
To further confirm the effect of wogonin on K562 cell differentiation, we examined the expression of glycophorin A (GPA) and CD71, two erythroid differentiation specific markers
The dosedependent increase of γ-globin further demonstrated the differentiation inducing activity of wogonin in K562 cells (Figure 1I). These results indicated that wogonin induced differentiation and arresting cell cycle at G0/G1 phase in K562 cells
Summary
The K562 cells were derived from a patient suffering from chronic myelogenous leukemia (CML) blast crisis phase and used as the cell line for the research of erythroid differentiation[1, 2]. Erythroid differentiation is a process of formation of red blood cells in the bone marrow is a highly regulated event. BCR-ABL has been verified to be the causative agent of CML. Imatinib is a BCR-ABL kinase inhibitor which blocks the growth of BCR-ABL-transformed cells, and is effective in disease remission in chronic phase CML patients [6,7,8]. Results from the ‘non-randomized stop IM’ trial showed that 61% of www.impactjournals.com/oncotarget
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