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KMID : 1195620230160020184
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Clinical and Experimental Otorhinolaryngology
2023 Volume.16 No. 2 p.184 ~ p.197
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Mitochondrial Ribosomal Protein L14 Promotes Cell Growth and Invasion by Modulating Reactive Oxygen Species in Thyroid Cancer
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Kim Hae-Jong
Quoc Khanh Nguyen
Jung Seung-Nam
Lim Mi-Ae
Oh Chan
Yudan Piao
YanLi Jin
Kim Ju-Hui
Kim Young-Il
Kang Yea-Eun
Chang Jae-Won
Koo Bon-Seok
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Abstract
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Objectives. The mitochondrial ribosomal protein L14 (MRPL14) is encoded by a nuclear gene and participates in mito-chondrial 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 CancerGenome Atlas (TCGA) and Chungnam National University Hospital (CNUH) databases. Functional studies ofMRPL14, including proliferation, migration, invasion, mitochondrial oxidative phosphorylation and reactive oxygenspecies (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 over-all mitoribosomal proteins (MRPs) compared with normal thyroid tissues. Of 78 MRPs, MRPL14 was highly ex-pressed 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 pro-moted cell migration via epithelial-mesenchymal transition-related proteins. Moreover, MRPL14 knockdown reducedthe expression of oxidative phosphorylation complex IV (MTCO1) and increased the accumulation of ROS. Cotreat-ment with a ROS scavenger restored cell proliferation and migration, which had been reduced by MRPL14 knock-down, 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 inthyroid cancer cells.
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KEYWORD
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Papillary Thyroid Cancer, Mitoribosomal Protein 14, Reactive Oxygen Species, Cancer Progression
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