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. 2022 Mar 25;13:846310. doi: 10.3389/fendo.2022.846310

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Copyright © 2022 Gilchrist and Echeverria

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Bone and Tumor Microenvironment. Bone and Tumor Microenvironment. BME produces RANKL, IL-3, and MIP-1α (CCL3) for OC activation. RANKL leads to the inhibition of OC apoptosis. IFN Type 1 secreted by MM cells favors MM growth and immunosuppression. CCL3 secreted by MM cells activate the MAPK pathway, further stimulating osteoclastogenesis. MM cells can inhibit OB differentiation with sclerostin and DKK1 by dysregulating the Wnt signaling pathway; an essential pathway for osteoblastogenesis. MM cells also secrete sFRP-2 which suppresses OB differentiation. MM cells inhibit Runx-2 in OB precursors and thus inhibit OB maturation. MM cells inhibit osteocytes via abnormal apoptosis by Notch signaling which is sustained by TNF-α. Crosstalk between BMSCs and MM cells induce pro-osteoclastogenic factors such as IL-6. MM cell secretion of CCL3 binds to CCR1 and CCR5 on OCs, enhancing OC activity.