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Article Abstract
Long noncoding RNAs (lncRNAs) play critical roles in tumor progression regulation, including osteosarcoma. Evidence indicates that N-methyladenosine (mA) modification modulates mRNA stability to regulate osteosarcoma tumorigenesis. Here, present research aims to detect the roles of mA-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 mA-modified site was found on the 3'-UTR of FOXD2-AS1, and mA 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 mA sites, forming a FOXD2-AS1/mA/FOXM1 complex to heighten FOXM1 mRNA stability. In conclusion, these findings propose a novel regulatory mechanism in which mA-modified FOXD2-AS1 accelerates the osteosarcoma progression through mA manner, which may provide new concepts for osteosarcoma tumorigenesis.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9161975 | PMC |
| http://dx.doi.org/10.1080/21655979.2021.2008218 | DOI Listing |
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