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Research: YOUN and COLLEAGUES,
Listed in Issue 293
Abstract
YOUN and COLLEAGUES, 1 Department of Integrative Bioscience and Biotechnology, Sejong University, Gwangjin-gu, Seoul, Korea; 2 Department of Molecular Biology, Dankook University, Cheonan-si, Chungnam, Korea; 3 Department of Biological Sciences, Pusan National University, Gumjeong-gu, Busan 46241, Republic of Korea studied at the molecular level the suppression of transcriptional action of Retinoic Acid (RA) in leukemia treatment.
Background
Retinoic acid (RA) has broad clinical applications for the treatment of various cancers, particularly acute promyelocytic leukemia.
Methodology
However, RA-based therapy is limited by relapse in patients associated with RA resistance, the mechanism of which is poorly understood. Here, we suggest a new molecular mechanism of RA resistance by a repressor, named RA resistance factor (RaRF). RaRF suppressed transcriptional activity of the RA receptor (RAR) by directly interacting with and sequestering RAR to the nucleolus in response to RA.
Results
RaRF was highly expressed in RA-resistant leukemia cells and its expression was strongly correlated with RA sensitivity. MCL1 was upregulated by RA treatment upon RaRF depletion, accompanying leukemic myeloblast differentiation, which is negatively regulated by ectopic RaRF expression.
Conclusion
Collectively, we propose that RaRF may be a factor in the resistance mechanism and thus a potential target for leukemia therapy using RA.
References
H Youn 1 , H-K Lee 1 , H-R Sohn 1 , U-H Park 1 , E-J Kim 2 , B Youn 3 , S-J Um 1.
RaRF confers RA resistance by sequestering RAR to the nucleolus and regulating MCL1 in leukemia cells. Oncogene. ;37(3):352-362. doi: 10.1038/onc.2017.329. Epub 2017 Sep 25. Jan 18 2018.
Comment
This research at the molecular level demonstrated that RA resistance factor (RaRF) suppressed transcriptional activity of the RA receptor (RAR) by directly interacting with and sequestering RAR to the nucleolus in response to RA. The authors we propose that RaRF may be a factor in the resistance mechanism and thus a potential target for leukemia therapy using Retinoic acid (RA).
