MAPK13 Promotes the Progression of Papillary Thyroid Cancer

Objective This study aims to analyze the genes that influence PTC progression, and investigate the role of MAPK13 in PTC. Methods Differentially expressed genes (DEGs) in Gene Expression Omnibus (GEO): GSE3467, GSE3678, GSE33630, and GSE58545 were analyzed between PTC and normal thyroid tissues. Then, univariate Cox regression and least absolute shrinkage and selection operator (LASSO) Cox regression analyses were performed on the DEGs using The Cancer Genome Atlas Program (TCGA) data. MAPK13 was subsequently identified to promote progress in PTC. The association between MAPK13 expression and clinicopathological features was analyzed using data from public database and collected cohort. The CCK-8 assay, EdU assay, wound healing assay, transwell assay, flow cytometry, GSEA enrichment analysis, and the xenograft model were used to investigate the function of MAPK13 in PTC. Results Higher expression of MAPK13 was associated with poorer progression-free survival, higher tumor pathologic stage, extrathyroid extension, lymph node metastasis, multifocal tumors, American Thyroid Association (ATA) stratification system level, and BRAF V600E mutation. Overexpression of MAPK13 significantly promoted cell proliferation, migration, and invasion and inhibited apoptosis of PTC. Knockdown of MAPK13 significantly inhibited cell proliferation, migration, and invasion, and promoted apoptosis of PTC. Epithelial-mesenchymal transition (EMT) was significantly enriched in GSEA analysis. The higher MAPK13 expression was related to higher N-cadherin and lower E-cadherin expression. Knockdown of MAPK13 significantly prevented tumor growth in vivo. Conclusion MAPK13 promotes the malignant biological behavior of PTC cells and associates with EMT. MAPK13 may be a potential biomarker of treatment.