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Title: MicroRNA-7 inhibits cell proliferation of chronic myeloid leukemia and sensitizes it to imatinib in vitro

Journal Article · · Biochemical and Biophysical Research Communications
 [1];  [2];  [1];  [2];  [1]
  1. Institute of Translational Medicine, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201620 (China)
  2. Shanghai Key Laboratory of Pancreatic Diseases, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201620 (China)

Highlights: • MiR-7 inhibits cell proliferation and induces apoptosis in CML. • MiR-7 sensitizes K562 cells to imatinib. • MiR-7 directly targets BCR-ABL/PI3K/AKT pathway. MicroRNA is a large class of non-coding small RNA that exerts critical roles in many physiological processes including cell proliferation. MicroRNA-7 (miR-7) has been considered as a tumor suppressor in most malignant tumors versus a tumor promoter in some other ones. However, its role in chronic myeloid leukemia remains unknown. Herein, we found that K562 cell proliferation was largely suppressed when it was stably transfected with miR-7. In accordance with that, apoptosis was also significantly upregulated in miR-7 stably-transfected K562 cells. Moreover, we found that miR-7-overexpressed K562 cells were far more sensitive to imatinib than controls. Further investigations showed that the ABL1 was a direct target of miR-7. Expression level of BCR-ABL and the activity of its downstream PI3K/AKT pathway were significantly reduced in miR-7-transfected cells. Taken together, our results showed that miR-7 inhibited proliferation and promoted apoptosis in K562 cells, and miR-7 might help to sensitize them to imatinib through BCR-ABL/PI3K/AKT signaling in chronic myeloid leukemia.

OSTI ID:
22897507
Journal Information:
Biochemical and Biophysical Research Communications, Vol. 494, Issue 1-2; Other Information: Copyright (c) 2017 Elsevier Inc. All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
Country of Publication:
United States
Language:
English