MiR-525-5p inhibits diffuse large B cell lymphoma progression via the Myd88/NF-κB signaling pathway

PeerJ. 2023 Nov 6:11:e16388. doi: 10.7717/peerj.16388. eCollection 2023.

Abstract

Diffuse large B-cell lymphoma (DLBCL) is a B-cell lymphoma with a high degree of aggressiveness. Recently, evidence has shown that miR-525-5p is decreased in DLBCL, suggesting its possible involvement in tumor progression. In this study, miR-525-5p suppressed proliferation, invasion and clonogenicity, and increased apoptosis of U2932 cells, whereas miR-525-5p silencing enhanced tumor cell growth. Next, miR-525-5p targets the 3'-UTR of Myd88, and Myd88 protein was increased in lymphoma tissues. Similar to the miR-525-5p mimic, Myd88 siRNA suppressed proliferation, invasion, and clonogenicity, and enhanced apoptosis of U2932 cells. We observed that Myd88 reversed the inhibitory effect of miR-525-5p on tumor cell growth by transfecting cells with miR-525-5p mimics alone or together with Myd88 overexpression vector. In addition, in vivo studies have shown that compared to the control group, U2932 cells with upregulated miR-525-5p expression have a reduced ability to induce tumor formation. In conclusion, our results demonstrate that miR-525-5p inhibits the progression of DLBCL through the Myd88/NF-κB pathway, which largely fills the gap of previous studies, and our results may provide a new reference for the targeted treatment of DLBCL.

Keywords: DLBCL; Invasion; MiR-525-5p; The Myd88/NF-κB pathway.

MeSH terms

  • Humans
  • Lymphoma, Large B-Cell, Diffuse* / genetics
  • MicroRNAs* / genetics
  • Myeloid Differentiation Factor 88 / genetics
  • NF-kappa B / genetics
  • Signal Transduction / genetics

Substances

  • NF-kappa B
  • MicroRNAs
  • Myeloid Differentiation Factor 88
  • MIRN525 microRNA, human

Grants and funding

This work is supported by the Beijing Life Oasis Public Welfare Service Center (cphcf-2022-15). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.