The mammalian acid chitinase promotes oncogenic properties of thyroid cancer cells through the JAK2/STAT3 pathway.

OBJECTIVE: Mammalian acid chitinase (AMCase; CHIA) has potential as a biomarker and drug target in the fields of medicine and pharmacology, and its role in inhibiting tumor growth and Th2 cell-mediated asthma-related inflammation has become a research hotspot. However, the role of CHIA in thyroid cancer is unclear. METHODS: Tissue microarrays and thyroid cancer cell lines were used to detect CHIA expression and determine its clinical relevance. CHIA gene expression was altered in thyroid cancer cells to examine the effects of CHIA expression on the biological behavior of thyroid cancer cells, and the related molecular mechanisms involved were explored. RESULTS: We first examined CHIA expression in a thyroid tissue microarray using immunohistochemistry. We found that CHIA was significantly upregulated in thyroid cancer tissues relative to paired thyroid cancer adjacent tissues. After correlation analysis, we found that upregulated CHIA expression correlated with the tumor-node-metastasis (TNM) stage of patients with thyroid cancer. Similarly, CHIA expression was significantly higher in the thyroid cancer cell lines BCPAP, TPC-1, KTC-1 and FTC133 than in the human normal thyroid epithelial cell line Nthy-ori-3-1. CHIA promotes proliferation, migration and invasion; inhibits thyroid cancer cell apoptosis; and regulates markers of proliferation and epithelial-mesenchymal transition. Mechanistically, CHIA activated the JAK2/STAT3 signaling pathway in thyroid cancer cells. CONCLUSIONS: CHIA upregulation promoted the proliferation, migration and invasion of thyroid cancer cells through JAK2/STAT3 signaling pathway activation. Therefore, CHIA could represent a potential new oncoprotein for patients with thyroid cancer.