Objectives@#. The mitochondrial
ribosomal protein L14 (MRPL14) is encoded by a nuclear
gene and participates in
mitochondrial protein translation. In this study, we aimed to investigate the
role of MRPL14 in
thyroid cancer. @*
Methods@#. We investigated the
association between MRPL14 expression and clinicopathological features using The
Cancer Genome Atlas (TCGA) and Chungnam National
University Hospital (CNUH) databases. Functional studies of MRPL14, including proliferation, migration, invasion, mitochondrial
oxidative phosphorylation and
reactive oxygen species (ROS)
production, were performed in
papillary thyroid cancer (PTC)
cell lines (B-CPAP and KTC-1). @*Results@#. Based on the TCGA
dataset, PTC
tissues lost mitochondrial integrity and showed dysregulated expression of overall mitoribosomal
proteins (MRPs) compared with normal
thyroid tissues. Of 78 MRPs, MRPL14 was highly expressed in
thyroid cancer tissues. MRPL14 overexpression was significantly associated with advanced
tumor stage, extrathyroidal extension, and
lymph node metastasis. MRPL14 increased
cell proliferation of
thyroid cancer and promoted
cell migration via
epithelial-mesenchymal transition-related
proteins. Moreover, MRPL14 knockdown reduced the expression of
oxidative phosphorylation complex IV (MTCO1) and increased the accumulation of ROS. Cotreatment with a ROS scavenger restored
cell proliferation and migration, which had been reduced by MRPL14 knockdown, implying that ROS functions as a key regulator of the oncogenic effects of MRPL14 in
thyroid cancer cells. @*Conclusion@#. Our findings indicate that MRPL14 may promote
cell growth, migration, and invasion by modulating ROS in
thyroid cancer cells.