Interference with KCNJ2 inhibits proliferation, migration and EMT progression of apillary thyroid carcinomacells by upregulating GNG2 expression.

Abstract

Papillary thyroid carcinoma is a common malignant tumor of the endocrine system. The specific role and molecular mechanism of potassium inwardly rectifying channel subfamily J member 2 (KCNJ2) in papillary thyroid carcinoma remain unknown. In the present study, the underlying mechanism of KCNJ2 in papillary thyroid carcinoma was explored. KCNJ2 expression in thyroid cancer tissues was predicted using the Gene Expression Profiling Interactive Analysis database, and reverse transcription-quantitative PCR and western blot analyses were performed to detect KCNJ2 expression in papillary thyroid carcinoma cell lines. Cell transfection was performed to inhibit KCNJ2 and G protein subunit γ2 (GNG2) expression. In addition, cell proliferation was detected via the colony formation and MTT assays. The wound healing and Transwell assays were performed to assess cell migration and invasion, respectively. Western blot analysis was performed to detect the expression levels of transport-related proteins and interstitial related proteins. The StarBase database was used to detect GNG2 expression in thyroid cancer. The results demonstrated that KCNJ2 expression was upregulated in papillary thyroid carcinoma cells. In addition, interfering with KCNJ2 expression inhibited the proliferation, invasion and migration of papillary thyroid carcinoma cells, and inhibited the epithelial-to-mesenchymal transition (EMT). These processes may be influenced by the upregulation of GNG2 expression induced by KCNJ2 knockdown. Overall, the results of the present study demonstrated that interference with KCNJ2 inhibited proliferation, migration and EMT progression of papillary thyroid carcinoma cells by upregulating GNG2 expression.