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Research: HE and COLLEAGUES,
Listed in Issue 291
Abstract
HE and COLLEAGUES, 1 Department of Pharmacy, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu, Sichuan, 611130, China; 2 Department of Pharmacy, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu, Sichuan, 611130, China. fuhl2005@sohu.com; 3 Department of Pharmacy, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu, Sichuan, 611130, China; zhixiang-yuan@hotmail.com showed that Dihydromyricetin (DMY), a 2,3-dihydroflavonol compound, exhibited a strong synergy with ATRA to promote APL NB4 cell differentiation.
Background
The success of all-trans retinoic acid (ATRA) in differentiation therapy for patients with acute promyelocytic leukemia (APL) highly encourages researches to apply a new combination therapy based on ATRA.
Methodology
Therefore, research strategies to further sensitize cells to retinoids are urgently needed. In this study, we showed that Dihydromyricetin (DMY), a 2,3-dihydroflavonol compound, exhibited a strong synergy with ATRA to promote APL NB4 cell differentiation.
Results
The authors observed that DMY sensitized the NB4 cells to ATRA-induced cell growth inhibition, CD11b expression, NBT reduction and myeloid regulator expression. PML-RARα might not be essential for DMY-enhanced differentiation when combined with ATRA, while the enhanced differentiation was dependent on the activation of p38-STAT1 signaling pathway.
Conclusion
Taken together, our study is the first to evaluate the synergy of DMY and ATRA in NB4 cell differentiation and to assess new opportunities for the combination of DMY and ATRA as a promising approach for future differentiation therapy. Copyright © 2017 Elsevier Inc. All rights reserved.
References
Ming-Hui He 1 , Qiang Zhang 1 , Gang Shu 1 , Ju-Chun Lin 1 , Ling Zhao 1 , Xiao-Xia Liang 1 , Lizi Yin 1 , Fei Shi 1 , Hua-Lin Fu 2 , Zhi-Xiang Yuan 3. Dihydromyricetin sensitizes human acute myeloid leukemia cells to retinoic acid-induced myeloid differentiation by activating STAT1 Biochem Biophys Res Commun.; 495(2): 1702-1707. doi: 10.1016/j.bbrc.2017.12.030. Epub 2017 Dec 7. Jan 8 2018.
