Downregulation of CDH16 in Papillary Thyroid Cancer and Its Potential Molecular Mechanism Analysed by qRT-PCR, TCGA and in silico Analysis

Abstract

Objective: Thyroid cancer has the highest prevalence among the cancer types that affect the endocrine system; however, its molecular mechanisms are not yet determined. Cadherin-16 (CDH16) plays an important role in the tumorigenesis of human cancers, but its influence on papillary thyroid cancer (PTC) is poorly investigated. This study aimed to explore the role of CDH16 in PTC. Methods: We performed quantitative real-time polymerase chain reaction to investigate CDH16 expression in PTC. The clinical significance of CDH16 expression in PTC was then evaluated using The Cancer Genome Atlas (TCGA) database. Bioinformatics analysis was also conducted to determine the potential molecular mechanisms of CDH16. Results: CDH16 was remarkably downregulated in PTC tumors compared with that in corresponding normal thyroid tissues in the local and TCGA cohorts. This downregulation was associated with unfavorable clinicopathological features, including histological type, high tumor stage, aggressive lymph node metastasis (LNM), and advanced clinical stage. In addition, logistic analyses revealed that the reduced expression of CDH16 can aggravate the risk of LNM in PTC. Bioinformatics analysis indicated that the co-expressed CDH16 genes mainly participated in signaling the cancer-related pathways. Conclusion: CDH16 is involved in PTC progression and acts as an LNM-related gene in PTC.