Role of tRNA-derived Fragments in the Mechanism of Thyroid Carcinoma
10.13471/j.cnki.j.sun.yat-sen.univ（med.sci）.2022.0312
- VernacularTitle:转运RNA衍生片段在甲状腺癌发病机制中的作用
- Author:
Miao-guan PENG
1
;
Ying-rong LAI
2
Author Information
1. Endocrinology and Metabolism Department， The Third Affiliated Hospital， Guangzhou Medical University， Guangzhou 510150， China
2. Department of pathology， The First Affiliated Hospital， Sun Yat-sen University， Guangzhou 510080， China
- Publication Type:Journal Article
- Keywords:
papillary thyroid carcinoma;
tRNA-derived fragments;
tumorigenesis
- From:
Journal of Sun Yat-sen University(Medical Sciences)
2022;43(3):437-448
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the expression of tRNA-derived fragments （tRFs） 3'tiR_026_GlnCTG （n） in PTC and its carcinogenic mechanism. MethodsFirst， two pairs of PTC and adjacent normal thyroid tissues were used for high-throughput microarray to screen differential tRFs. Based on the microarray results， we verified the expression of significantly different tRFs in 10 pairs of PTC and adjacent normal thyroid tissues. Then， we increased sample sizes and verified the expression of 3'tiR_026_GlnCTG （n） in another 46 pairs of PTC and adjacent normal thyroid tissues by Quantitative PCR （qPCR）. Mimics of3'tiR_026_GlnCTG （n） were transfected into PTC cell lines. The expression level was verified by quantitative reverse transcription polymerase chain reaction （qRT-PCR） and the transfection was confirmed. Meanwhile， the transfected cell lines were lysed， protein was extracted， incubated with relevant antibodies including the MEK/ERK/p90RSK signaling pathway and the western blotting was performed. Results3'tiR_026_GlnCTG （n） is one of the most significantly upregulated tRFs between PTC tissues and adjacent normal tissues. Overexpression of 3'tiR_026_GlnCTG （n） promoted migration， invasion and proliferation in KTC1 and BCPAP cells. MEK/ERK pathway inhibitors decrease the migration， invasion and proliferation in KTC1 and BCPAP cells. The phosphorylation of MEK， ERK and their downstream target p90RSK was significantly increased in 3'tiR_026_GlnCTG （n）-overexpressing cells. Conclusions3'tiR_026_GlnCTG （n） might play a key oncogenic role in PTC tumorigenesis and development by activating the MEK/ERK/p90RSK pathway. It will provide new insight into the pathogenesis of PTC and may lead to effective therapeutic strategies.
