2. Academic Validation
  3. Midkine and TNFSF10 as downstream molecules of type I interferon are involved in the treatment of myelofibrosis

Midkine and TNFSF10 as downstream molecules of type I interferon are involved in the treatment of myelofibrosis

  • Biochim Biophys Acta Gen Subj. 2025 Sep 29;1869(12):130863. doi: 10.1016/j.bbagen.2025.130863.
Yaoyao Chen 1,  Fanxiang Yin 2,  Xiaoqian Wang 3,  Huilin Zhang 4,  Ping Tang 5,  Mengjiao Xue 2,  Nannan Sun 5,  Jin Li 4,  Chang Chen 1,  Bingjie Wang 1,  Qingxuan Xin 6,  Juanxia Zhou 5,  Yingmei Li 5,  Shuya Wang 7,  Shaohua Yan 2,  Jiani Li 4,  Yunling Zhu 8,  Bo Qin 2,  Baohong Yue 9,  Yong Jiang 10,  Rongqun Guo 11
Affiliations

Affiliations

  • 1 Translational Medical Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China; Department of Laboratory Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
  • 2 Translational Medical Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
  • 3 Department of Laboratory Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
  • 4 Translational Medical Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China; Department of Hematology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
  • 5 Department of Hematology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
  • 6 Department of Laboratory Medicine, The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, Henan, China.
  • 7 Department of Blood Transfusion, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
  • 8 Translational Medical Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China; Department of Emergency Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
  • 9 Department of Hematology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China. Electronic address: fccybh@zzu.edu.cn.
  • 10 Henan International Joint Laboratory of Infection and Immunity, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, Henan, China; Henan Key Laboratory of Critical Care Medicine, Department of Emergency Medicine, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, Henan, China; Institute of Infection and Immunity, Henan Academy of Innovations in Medical Science, Zhengzhou, Henan, China. Electronic address: jiang48231@163.com.
  • 11 Translational Medical Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China; Department of Emergency Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China. Electronic address: guorq2007@163.com.
PMID: 41033419 DOI: 10.1016/j.bbagen.2025.130863
Abstract

Myelofibrosis (MF), a myeloproliferative neoplasm, remains incurable for most patients. Although some individuals are eligible for allogeneic hematopoietic stem cell transplantation, current therapies generally slow disease progression rather than achieve a cure. In this study, we found that type I interferon (IFN) treatment enhances midkine (MDK) expression, and MDK is involved in the differentiation and maturation of progenitor cells. Notably, MDK treatment drives tumor cells into the cell cycle, thereby increasing the therapeutic effect of busulfan. Furthermore, MDK promotes osteogenic differentiation of mesenchymal stem cells (MSC), contributing to the remodeling of the bone marrow microenvironment. In addition, type I IFN upregulates TNFSF10, leading to tumor cell death through mutual killing.

Keywords

Bone marrow microenvironment; Midkine; Myelofibrosis; TNFSF10; Type-I interferon.

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