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LILRB4 regulates multiple myeloma development through STAT3-PFKFB1 pathway.

Li Xie1, Chiqi Chen1, Tinghua Zhang1

  • 1Hongqiao International Institute of Medicine, Shanghai Tongren Hospital, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Faculty of Basic Medicine, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.

Cell Death & Disease
|July 18, 2024
PubMed
Summary

Leukocyte immunoglobulin-like receptor B4 (LILRB4) is highly expressed in multiple myeloma, hindering immunotherapy. Targeting LILRB4 shows potential as a new therapeutic strategy for multiple myeloma patients.

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Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Multiple myeloma (MM) exhibits variable responses to immunotherapy, necessitating novel therapeutic targets.
  • Existing immunotherapies are insufficient for all MM patients, with some remaining unresponsive or experiencing relapse.

Purpose of the Study:

  • To investigate the role of leukocyte immunoglobulin-like receptor B4 (LILRB4) in multiple myeloma progression.
  • To explore LILRB4 as a potential therapeutic target for enhancing MM immunotherapy.

Main Methods:

  • Analysis of LILRB4 expression in MM cell lines and patient samples.
  • In vitro and in vivo knockdown of LILRB4 to assess its effect on MM cell growth.
  • Investigation of the molecular mechanisms involving IKZF1, STAT3, and PFKFB1 pathways.
  • Evaluation of LILRB4-blocking antibodies for therapeutic potential.

Main Results:

  • LILRB4 expression was significantly elevated in MM cell lines and patient samples.
  • High LILRB4 expression correlated inversely with overall survival in MM patients.
  • LILRB4 knockdown suppressed MM cell proliferation both in vitro and in vivo.
  • IKZF1 was identified as a transactivator of LILRB4, which in turn activates STAT3-PFKFB1 signaling to promote MM cell proliferation.
  • Blocking LILRB4 signaling with antibodies inhibited MM progression.

Conclusions:

  • LILRB4 is a key driver of MM cell proliferation and progression.
  • Targeting LILRB4 represents a promising novel therapeutic strategy for multiple myeloma immunotherapy.