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Circ-METTL15 stimulates the aggressive behaviors of papillary thyroid cancer cells by coordinating the miR-200c-3p/XIAP axis.

Authors :
YUHAO HUANG
XINYU ZENG
YANLING CAI
YAN YANG
YUJIE ZHANG
Source :
Turkish Journal of Biology. 2024, Vol. 48 Issue 2, p142-152. 11p.
Publication Year :
2024

Abstract

Background/aim: Papillary thyroid carcinoma (PTC) is the most common form of thyroid cancer. The critical importance of circular RNA (circRNA) in a range of cancer types has been lately recognized. However, research on the functions of circRNAs in PTC has been limited thus far. Therefore, this research aimed at exploring the function and mechanism of circ-methyltransferase-like 15 (METTL15) in PTC cells. Materials and methods: Quantitative measurements of circ-METTL15, miR-200c-3p, and X-linked inhibitor of apoptosis protein (XIAP) in PTC cells were conducted using reverse transcription-quantitative polymerase chain reaction or Western blot analysis. To investigate cell growth, cell counting kit-8 and colony formation tests were employed, apoptosis was analyzed using flow cytometry, and migration and invasion were studied through Transwell assays. The targeted binding sites between miR-200c-3p and circ-METTL15 or XIAP were predicted by starBase and then verified by dual luciferase reporter assay. Results: circ-METTL15 and XIAP were upregulated in the PTC cells, while miR-200c-3p was downregulated. Downregulating circ- METTL15 or upregulating miR-200c-3p resulted in inhibited proliferation, migration, and invasion of PTC cells, while promoting apoptosis. miR-200c-3p was the downstream molecule of circ-METTL15, and XIAP was the direct target of miR-200c-3p. Forcing XIAP expression obstructed circ-METTL15 silencing to inhibit PTC cell activity. Conclusion: By coopting miR-200c-3p/XIAP, Circ-METTL15 stimulates aggressive behavior in PTC cells. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
13000152
Volume :
48
Issue :
2
Database :
Academic Search Index
Journal :
Turkish Journal of Biology
Publication Type :
Academic Journal
Accession number :
177175589
Full Text :
https://doi.org/10.55730/1300-0152.2690