Galectin-3 (gal-3) is an integral protein in gliomagenesis that has been implicated in a myriad of oncogenic processes such as metabolic adaptation, angiogenesis, and tumor invasiveness. Gal-3 also has a well characterized role as a harbinger of inflammation, inducing the release of pro-inflammatory cytokines including interleukin-1 beta (IL-1B) and interleukin 6 (IL-6). However, these findings have not been well translated to oncology to date. Data from The Cancer Genome Atlas (TCGA) shows that gal-3 is highly overexpressed in low grade gliomas as well as glioblastoma (n = 156) compared to healthy brain tissue (n = 5). Further analysis of data from the Chinese Glioma Genome Atlas shows high expression of gal-3, IL-1B, and Il-6 are each associated with significantly (p < 0.001) worse survival in gliomas. Additionally, the expression of gal-3 is significantly correlated with both IL-1B and IL-6 expression across all malignant gliomas. In other cancers including neuroblastoma it has been shown that IL-6 expression is largely dependent upon gal-3 signaling pathways. This has been shown with regards to IL-1B as well, a molecule which along with IL-6 has been well described for promoting angiogenesis and metastasis. Given these cytokines' highly correlated expression to gal-3 in gliomas, it is likely that gal-3 is involved in inducing cytokine expression in glioma. Here we will discuss the myriad of signaling pathways through which gal-3 induces inflammatory cytokine release in cancer, the implications of these pathways on glioma progression, and the therapeutic potential of targeting this axis.

Citation Format: John Caniglia. Expression of galectin-3 and pro-inflammatory cytokines in gliomas: Implications and therapeutic potential [abstract]. In: Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; 2021 Oct 5-6. Philadelphia (PA): AACR; Cancer Immunol Res 2022;10(1 Suppl):Abstract nr P029.