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2. N6-methyladenosine methyltransferase WTAP-stabilized FOXD2-AS1 promotes the osteosarcoma progression through m6A/FOXM1 axis

Author

Ren, Zhipeng, Hu, Yongcheng, Sun, Jie, Kang, Yuxiang, Li, Guishi, and Zhao, Hejun

Subjects
Bioengineering, General Medicine, Applied Microbiology and Biotechnology, Biotechnology
Abstract

Long noncoding RNAs (lncRNAs) play critical roles in tumor progression regulation, including osteosarcoma. Evidence indicates that N6-methyladenosine (m6A) modification modulates mRNA stability to regulate osteosarcoma tumorigenesis. Here, present research aims to detect the roles of m6A-modified lncRNA FOXD2-AS1 in the osteosarcoma pathophysiological process. Clinical data unveiled that osteosarcoma patients with higher FOXD2-AS1 expression had a poorer overall survival rate compared to those with lower FOXD2-AS1 expression. Functional research illuminated that FOXD2-AS1 accelerated the migration, proliferation and tumor growth in vitro and in vivo. Mechanistically, a remarkable m6A-modified site was found on the 3ʹ-UTR of FOXD2-AS1, and m6A methyltransferase WTAP (Wilms’ tumor 1 associated protein) promoted the methylation modification, thus enhancing the stability of FOXD2-AS1 transcripts. Furthermore, FOXD2-AS1 interacted with downstream target FOXM1 mRNA through m6A sites, forming a FOXD2-AS1/m6A/FOXM1 complex to heighten FOXM1 mRNA stability. In conclusion, these findings propose a novel regulatory mechanism in which m6A-modified FOXD2-AS1 accelerates the osteosarcoma progression through m6A manner, which may provide new concepts for osteosarcoma tumorigenesis.

Published
2022

6. N 6 -methyladenosine methyltransferase WTAP-stabilized FOXD2-AS1 promotes the osteosarcoma progression through m 6 A/FOXM1 axis.

Author

Ren Z, Hu Y, Sun J, Kang Y, Li G, and Zhao H

Subjects
3' Untranslated Regions, Adenosine analogs & derivatives, Carcinogenesis genetics, Cell Cycle Proteins genetics, Cell Line, Tumor, Cell Proliferation genetics, Forkhead Box Protein M1 genetics, Forkhead Box Protein M1 metabolism, Gene Expression Regulation, Neoplastic, Humans, Methyltransferases genetics, Methyltransferases metabolism, RNA Splicing Factors genetics, Bone Neoplasms genetics, Osteosarcoma genetics, Osteosarcoma pathology, RNA, Long Noncoding genetics, RNA, Long Noncoding metabolism
Abstract

Long noncoding RNAs (lncRNAs) play critical roles in tumor progression regulation, including osteosarcoma. Evidence indicates that N 6 -methyladenosine (m 6 A) modification modulates mRNA stability to regulate osteosarcoma tumorigenesis. Here, present research aims to detect the roles of m 6 A-modified lncRNA FOXD2-AS1 in the osteosarcoma pathophysiological process. Clinical data unveiled that osteosarcoma patients with higher FOXD2-AS1 expression had a poorer overall survival rate compared to those with lower FOXD2-AS1 expression. Functional research illuminated that FOXD2-AS1 accelerated the migration, proliferation and tumor growth in vitro and in vivo. Mechanistically, a remarkable m 6 A-modified site was found on the 3'-UTR of FOXD2-AS1, and m 6 A methyltransferase WTAP (Wilms' tumor 1 associated protein) promoted the methylation modification, thus enhancing the stability of FOXD2-AS1 transcripts. Furthermore, FOXD2-AS1 interacted with downstream target FOXM1 mRNA through m 6 A sites, forming a FOXD2-AS1/m 6 A/FOXM1 complex to heighten FOXM1 mRNA stability. In conclusion, these findings propose a novel regulatory mechanism in which m 6 A-modified FOXD2-AS1 accelerates the osteosarcoma progression through m 6 A manner, which may provide new concepts for osteosarcoma tumorigenesis.

Published
2022
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