YTHDC2 Retards Cell Proliferation and Triggers Apoptosis in Papillary Thyroid Cancer by Regulating CYLD-Mediated Inactivation of Akt Signaling

N6-Methyladenosine (m 6 A) mRNA methylation modification is regarded as an important mechanism involved in diverse physiological processes. YT521-B homology (YTH) domain family members are associated with the tumorigenesis of several cancers. However, the role of YTHDC2 in papillary thyroid cancer (...

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Bibliographic Details
Published in:Applied biochemistry and biotechnology 2024, Vol.196 (1), p.588-603
Main Authors: Zhou, Guangying, Wang, Shasha
Format: Article
Language:English
Subjects:
AKT protein
Apoptosis
BAX protein
Bcl-2 protein
Biochemistry
Biotechnology
Cancer
Caspase-3
Cell growth
Cell proliferation
Chemistry
Chemistry and Materials Science
Deactivation
Homology
Inactivation
Kinases
Lymphoma
Methylation
mRNA
N6-methyladenosine
Original Article
Papillary thyroid cancer
RNA modification
Thyroid
Thyroid cancer
Tumorigenesis
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Summary:N6-Methyladenosine (m 6 A) mRNA methylation modification is regarded as an important mechanism involved in diverse physiological processes. YT521-B homology (YTH) domain family members are associated with the tumorigenesis of several cancers. However, the role of YTHDC2 in papillary thyroid cancer (PTC) progression remains unknown. Results showed that YTHDC1, YTHDF1, YTHDF2, and YTHDF3 showed no observable difference in thyroid cancer samples. YTHDC2 was significantly downregulated in thyroid cancer samples and cells. YTHDC2 inhibited cell proliferation in PTC cells. YTHDC2 elicited apoptosis in PTC cells, as demonstrated by the elevated expression of pro-apoptotic factors cl-caspase-3/caspase-3 and Bcl-2-associated (Bax), and the reduced anti-apoptotic B cell lymphoma-2 (Bcl-2) expression. There was a positive correlation between YTHDC2 and cylindromatosis (CYLD) expression based on GEPIA database. YTHDC2 increased CYLD expression in PTC cells. CYLD knockdown abolished the effects of YTHDC2 on PTC cell proliferation and apoptosis. Additionally, YTHDC2 inactivated the protein kinase B (Akt) pathway by increasing CYLD in PTC cells. Overall, YTHDC2 inhibited cell proliferation and induced apoptosis in PTC cells by regulating CYLD-mediated inactivation of Akt pathway.
ISSN:0273-2289
1559-0291
DOI:10.1007/s12010-023-04540-8