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. 2021 Nov 23;11(12):1282. doi: 10.3390/life11121282

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© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Illustration of the underlying mechanisms of the CXCL13/CXCR5 axis in cell fate determination. The CXCL13/CXCR5 axis triggers multiple intracellular signal transduction pathways. After CXCL13 binds to CXCR5, G proteins dissociate from CXCR5, dividing into Gα and Gβγ, thereby inducing different downstream molecular events [20,23]. CXCL13 promotes osteogenic differentiation by inhibiting miRNA-23a, inducing ALP activity, and calcium node formation [82]. Upregulation of MMPs, N-cadherin, Vimentin, Slug, and Snail, and downregulation of E-cadherin under CXCL13 treatment enhances tumor cell migration [18,83]. The CXCL13/CXCR5 axis activates PI3K/Akt, integrin-β3/Src/Paxillin/FAK, and the DOCK/JNK pathway to induce cell survival, invasion, and proliferation, respectively [73]. CXCL13 increases the phosphorylation of c-Myc and c-Jun, and upregulates the transcriptional regulator NFATc3, which binds to the promoter region of RANKL and elevates the expression of RANKL [74,84]. ALP, alkaline phosphatase; Ca, calcium; MMPs: matrix metalloproteinase; BAD, Bcl-2 agonist of cell death; FAK, focal adhesion kinase; DOCK2, dedicator of cytokinesis 2; JNK, c-Jun kinase; RANKL, receptor activator of NF-kB ligand.