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Updated: May 10, 2025

The Soft Agar Colony Formation Assay
Published on: October 27, 2014
The m6A modification of LncRNA LINC00200 regulated by WTAP accelerates glioma tumorigenesis by regulating
Zhiying Lu1, Jing Chen1, Chao Luo2
1Department of Pediatrics, Wuhan Fourth Hospital, No.76, Jiefang Avenue, Qiaokou District, Wuhan, 430034, Hubei, China.
Background:
Several studies have delineated that dysregulated N6-methyladenosine (m6A) regulators participate in glioma progression. The objective of this study is to investigate the mechanism of Wilms' tumor 1-associating protein (WTAP)-mediated m6A modification of long noncoding RNA (lncRNA) LINC00200 in glioma.
Methods:
The LINC00200 expression in glioma was analyzed by qRT-PCR. The expressions of WTAP and Wnt/β-catenin pathway associated proteins were determined via qRT-PCR or western blotting. The levels of WTAP-mediated m6A modification of LINC00200 was ascertained by MeRIP-qPCR. Functionally, the effects of LINC00200 knockdown and the interaction of WTAP with LINC00200 on the glioma cell characteristics were examined by CCK8, colony formation, and transwell migration/invasion assays. In vivo experiments were performed to verify the effect of LINC00200 on tumor growth.
Results:
LINC00200 was overexpressed in glioma, and high LINC00200 level was related to higher-grade tumor. Moreover, its knockdown inhibited the malignant properties and expression of molecules related to Wnt/β-catenin pathway in glioma cell lines. In vivo, LINC00200 knockdown attenuated tumor growth. WTAP was also overexpressed in glioma tissues and demonstrated a positive association with LINC00200 expression. Furthermore, the relative enrichment of LINC00200 m6A was enhanced/reduced in a WTAP-dependent manner. Meanwhile, silencing LINC00200 partially reversed the malignant effects of WTAP overexpression in glioma.
Conclusion:
These results demonstrate that WTAP-mediated m6A modification of LINC00200 promotes glioma progression by modulating Wnt/β-catenin pathway.
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