FAM20C Promotes Papillary Thyroid Cancer Proliferation and Metastasis via Epithelial–Mesenchymal Transition

Abstract

Thyroid cancer (TC) is the prevailing malignancy that impacts the endocrine system, accounting for 1% of all recently diagnosed malignancies in humans. The incidence of TC has been continuously increasing, which can be attributed to advancements in clinical diagnostic technology. However, the mechanisms behind the development of TC are still not well understood. TC is classified into four pathological forms: medullary thyroid cancer, papillary thyroid cancer (PTC), follicular thyroid cancer, and poorly differentiated TC. PTC constitutes more than 80% of all TC cases globally. Current research indicates that complex genetic and cellular processes could be responsible for the growth and spread of TC. Next‐generation sequencing (RNA‐seq) of 79 PTC samples and their corresponding normal thyroid tissues was performed to investigate the molecular mechanisms of PTC. An analysis of RNA‐seq data from a local cohort from The Cancer Genome Atlas (TCGA) revealed that, compared with normal tissues, PTC tissues presented elevated FAM20C expression levels. In vitro, the function of FAM20C was validated with small interfering RNA (siRNA). Gene set enrichment analysis (GSEA) revealed the pathways influenced by FAM20C. A western blot experiment was used to investigate protein expression levels associated with epithelial‒mesenchymal transition (EMT). In conclusion, by regulating EMT, FAM20C facilitates PTC cell proliferation and metastasis.