LGALS2 suppresses the progression of papillary thyroid carcinoma by regulating the PI3K/AKT pathway.

Background: The galectin 2 (LGALS2) protein has been shown to be associated with the pathogenic progression of a range of cancer types, yet its role in papillary thyroid carcinoma (PTC) remains poorly defined. Accordingly, the present study was conducted to address this gap in the literature. Methods: Eighty pairs of tumor and paracancerous tissues from PTC patients were collected. Western immunoblotting and real-time quantitative polymerase chain reaction (qPCR) were used to compare LGALS2 expression levels in tumor and paracancerous tissues from PTC patients. An LGALS2 overexpression construct was produced by inserting the coding sequence for this gene into a pcDNA4.0 vector, and LGALS2-specific and control siRNA constructs were obtained. CCK-8, EdU uptake, and apoptotic assays were used to gauge the role of LGALS2 as a regulator of Results: LGALS2 mRNA and protein levels were reduced in both PTC tumors and cell lines, and the expression of this gene was related to PTC patient prognosis and clinicopathological features. LGALS2 knockdown enhanced PTC cell proliferative activity while decreasing the sensitivity of these cells to apoptotic death. In contrast, the opposite effect was evident following LGALS2 overexpression Conclusions: These data indicate that LGALS2 suppresses PTC progression via PI3K/AKT pathway activation, suggesting that LGALS2 offers value as a treatment target for patients with this cancer type.