Effect of Plumbagin on growth inhibition and apoptosis of imatinib-resistant chronic myeloid leukemia

Chỉ số đề mục

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BB

Tác giả

Bui Thi Kim Ly, Hoang Thanh Chi, Quach Ngo Diem Phuong, Ho Bao Thuy Quyen, Quách Ngô Diễm Phương⁽¹⁾

Nhan đề

Effect of Plumbagin on growth inhibition and apoptosis of imatinib-resistant chronic myeloid leukemia

Nhan đề tiếng anh

Effect of Plumbagin on growth inhibition and apoptosis of imatinib-resistant chronic myeloid leukemia

Nguồn trích

Ho Chi Minh City Open University Journal of Science: Engineering and Technology

Năm xuất bản

2017

Số

1

Trang

ISSN

Từ khóa

Từ khóa tiếng anh

Tóm tắt

Development of a new inhibitor of BCR-ABL tyrosine kinase is necessary for the treatment of chronic myeloid leukemia (CML) because of increasing resistance and tolerance to Imatinid efforts. Herein, we reported Plumbagin can significantly inhibit the growth of CML. The results revealed that Plumbagin inhitbited TCCY and TCCY/T315I cells with IC50 values 3 μM and 2.1 μM, respectively. Plumbagin also showed anti-proliferative effects on both the wide type Ba/F3 and the BCR-ABL-transfected Ba/F3 cells with a range of IC50 from 3.2 to 3.8 μM. In addition, Plumbagin induced the apoptosis of CML cells. That would provide a new and potential drug as a chemotherapy medication in the treatment of Imatinid -resistant CML.

Tóm tắt tiếng anh

Development of a new inhibitor of BCR-ABL tyrosine kinase is necessary for the treatment of chronic myeloid leukemia (CML) because of increasing resistance and tolerance to Imatinid efforts. Herein, we reported Plumbagin can significantly inhibit the growth of CML. The results revealed that Plumbagin inhitbited TCCY and TCCY/T315I cells with IC50 values 3 μM and 2.1 μM, respectively. Plumbagin also showed anti-proliferative effects on both the wide type Ba/F3 and the BCR-ABL-transfected Ba/F3 cells with a range of IC50 from 3.2 to 3.8 μM. In addition, Plumbagin induced the apoptosis of CML cells. That would provide a new and potential drug as a chemotherapy medication in the treatment of Imatinid -resistant CML.

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