AI Article Synopsis
- STAT3 is a transcription factor linked to poor prognosis in diffuse large B-cell lymphoma (DLBCL) and may serve as a therapeutic target.
- The study found that STAT3 activates the transcription of CCL4, which in turn triggers the Wnt/β-catenin pathway, contributing to cancer progression.
- Silencing STAT3 in DLBCL cells reduced tumor growth and malignancy, presenting it and CCL4 as potential biomarkers for DLBCL treatment.
Article Abstract
Signal transducer and activator of transcription 3 (STAT3) is a transcription factor and a candidate therapeutic option for human cancers. However, the underlying mechanism of STAT3 in the pathogenesis of diffuse large B-cell lymphoma (DLBCL) is yet to be established. We studied here whether STAT3 contributes to C-C motif chemokine ligand (CCL4) transcription elevation in DLBCL. Our established protein-protein interactions network revealed the overexpression of STAT3 and CCL4 in DLBCL. Mechanistically, STAT3 activated CCL4 transcription to induce the Wnt/β-catenin pathway. The prognostic analysis exhibited that the overall survival of patients with high STAT3 and CCL4 were poorer than those with low STAT3 and CCL4 expression. In addition, silencing of STAT3 reverted the malignant phenotype in DLBCL cells. CCL4 overexpression partly weakened the si-STAT3-mediated antitumor effects on DLBCL cells. Tumor xenograft models showed that si-STAT3 inhibited tumor growth in vivo and decreased proliferative and mitogenic activities in tumor tissues, which was consistent with the in vitro data. Hence, this study provides new evidence that STAT3 and CCL4 may be new prognostic biomarkers and therapeutic targets for treating DLBCL.
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| http://dx.doi.org/10.1159/000521445 | DOI Listing |
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