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Published on: August 23, 2019
LGALS2 suppresses the progression of papillary thyroid carcinoma by regulating the PI3K/AKT pathway
Debin Xu1, Liangyun Guo2, Shuyong Zhang1
1Department of Thyroid and Neck Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
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 in vitro PTC cell growth and apoptosis, while its in vivo role was assessed using a murine xenograft model.
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 in vitro and in vivo. LGALS2 also suppressed the progression of PTC by its ability to induce phosphatidylinositol-3-kinase/protein kinase B (PI3K/AKT) pathway activation.
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.
Insights
Galectin 2 (LGALS2) suppresses papillary thyroid carcinoma (PTC) progression by activating the PI3K/AKT pathway. Reduced LGALS2 expression correlates with poor prognosis, highlighting its potential as a therapeutic target in PTC.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- The role of galectin 2 (LGALS2) in papillary thyroid carcinoma (PTC) pathogenesis is not well understood.
- LGALS2 is implicated in the progression of various cancers, necessitating investigation in PTC.
Purpose of the Study:
- To investigate the role and mechanism of LGALS2 in papillary thyroid carcinoma (PTC).
- To determine if LGALS2 expression levels correlate with PTC patient prognosis and clinicopathological features.
Main Methods:
- Compared LGALS2 expression in 80 PTC tumor and paracancerous tissues using Western immunoblotting and qPCR.
- Assessed LGALS2's role in PTC cell growth, apoptosis, and tumor progression in vitro and in vivo using overexpression and knockdown constructs.
- Investigated the involvement of the PI3K/AKT pathway in LGALS2-mediated effects.
Main Results:
- LGALS2 mRNA and protein levels were significantly reduced in PTC tumors and cell lines.
- LGALS2 expression correlated with PTC patient prognosis and clinicopathological features.
- LGALS2 suppressed PTC cell proliferation and apoptosis, and inhibited tumor growth in vivo, by activating the PI3K/AKT pathway.
Conclusions:
- LGALS2 acts as a tumor suppressor in PTC by activating the PI3K/AKT pathway.
- Reduced LGALS2 expression is associated with unfavorable prognosis in PTC patients.
- LGALS2 represents a promising therapeutic target for papillary thyroid carcinoma.
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