The Role of Rarely Studied Chemokines in Tumor Progression in Multiple Myeloma (MM)

TL;DR

This paper reviews the role of under-researched chemokines in multiple myeloma tumor progression and their effects on bone destruction and immune cell recruitment.

Contribution

The paper highlights the underexplored roles of specific chemokines in multiple myeloma and their potential as therapeutic targets.

Findings

Lesser-known chemokines like CXCL13 and CCL2 influence bone destruction and angiogenesis in MM.

These chemokines affect immune cell recruitment and chemoresistance in the MM tumor niche.

Bioinformatic analysis suggests these chemokines could be viable targets for MM therapy.

Abstract

This review compiles current knowledge on the significance of lesser-known chemokines in multiple myeloma (MM) tumor processes, including CXCL13, CCR2 ligands (CCL2 [MCP-1], CCL7 [MCP-3]), CCL4, CCL5 (RANTES), CCL17, CCL20, CCL27, CCL28, and CX3CL1 (fractalkine). It describes their impact on bone destruction, bone marrow angiogenesis, chemoresistance, and the recruitment of cells into the MM niche, such as macrophages, myeloid-derived suppressor cells, and cytotoxic lymphocytes, along with their effects on mesenchymal stromal cells.

Multiple myeloma (MM) is a plasma cell neoplasm. Studies of chemokines in MM pathogenesis have primarily focused on CCR1 ligands such as CCL3 (MIP-1α), CXCL12 and its receptor CXCR4, as well as CXCR2 and CXCR3 ligands. However, the roles of the remaining 30 chemokines have been investigated much less frequently. This review compiles current knowledge on the significance of lesser-known chemokines in MM tumor processes, including CXCL13, CCR2 ligands (CCL2 [MCP-1], CCL7 [MCP-3]), CCL4, CCL5 (RANTES), CCL17, CCL20, CCL27, CCL28, and CX3CL1 (fractalkine). It describes their impact on bone destruction, bone marrow angiogenesis, chemoresistance, and the recruitment of cells into the MM niche, such as macrophages, myeloid-derived suppressor cells, and cytotoxic lymphocytes, along with their effects on mesenchymal stromal cells. A bioinformatic analysis highlights the significance of these chemokines in MM, and the possibility of targeting them in MM therapy is also considered.

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