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Neuropeptide Y improves cisplatin-induced bone marrow dysfunction without blocking chemotherapeutic efficacy in a cancer mouse model
Jae-sung Bae1,2,3,*,#, Min Hee Park1,2,3, In Kyung Jung1,2,3, Woo-Kie Min4, Jin Ho Choi5, Gyu Man Kim6, Hee Kyung Jin1,7,#
1Stem Cell Neuroplasticity Research Group, Kyungpook National University,
2Department of Physiology, School of Medicine, Kyungpook National University,
3Department of Biomedical Science, BK21 Plus KNU Biomedical Convergence Program, Kyungpook National University,
4Department of Orthopaedic Surgery, Kyungpook National University Hospital,
5Department of Mechanical Engineering, Gumi University,
6School of Mechanical Engineering and 7College of Veterinary Medicine, Kyungpook National University
Cisplatin is the most effective and widely used chemotherapeutic agent for many types of cancer. Unfortunately, its clinical use is limited by its adverse effects, notably bone marrow suppression leading to abnormal hematopoiesis. We previously revealed that neuropeptide Y (NPY) is responsible for the maintenance of hematopoietic stem cell (HSC) function by protecting the sympathetic nervous system (SNS) fibers survival from chemotherapy-induced bone marrow impairment. Here, we show the NPY-mediated protective effect against bone marrow dysfunction due to cisplatin in an ovarian cancer mouse model. During chemotherapy, NPY mitigates reduction in HSC abundance and destruction of SNS fibers in the bone marrow without blocking the anticancer efficacy of cisplatin, and it results in the restoration of blood cells and amelioration of sensory neuropathy. Therefore, these results suggest that NPY can be used as a potentially effective agent to improve bone marrow dysfunction during cisplatin-based cancer therapy.
Abstract, Accepted Manuscript(in press) [Submitted on June 13, 2017, Accepted on July 7, 2017]
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