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Long noncoding RNA UBA6-AS1 inhibits the malignancy of ovarian cancer cells via suppressing the decay of UBA6 mRNA

Ovarian cancer (OC) is one of the most common cancer in women worldwide. A recent study reported that long noncoding RNA (lncRNA) Ubiquitin like modifier activating enzyme 6 antisense RNA 1 (UBA6-AS1) is significantly correlated with the prognosis of patients with OC and also involved in N(6)-methyl...

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Detalles Bibliográficos
Autores principales: Wang, Yaogang, Chen, Zhigao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8805991/
https://www.ncbi.nlm.nih.gov/pubmed/34951345
http://dx.doi.org/10.1080/21655979.2021.2011640
Descripción
Sumario:Ovarian cancer (OC) is one of the most common cancer in women worldwide. A recent study reported that long noncoding RNA (lncRNA) Ubiquitin like modifier activating enzyme 6 antisense RNA 1 (UBA6-AS1) is significantly correlated with the prognosis of patients with OC and also involved in N(6)-methyladenosine (m(6)A) regulation. However, its influence on OC progression and the underlying mechanism is still not well demonstrated. Here, we found that UBA6-AS1 directly associated with UBA6 mRNA and inhibited its decay. Further mechanism investigation revealed that UBA6-AS1 increased the m(6)A methylation of UBA6 mRNA via recruiting RNA binding motif protein 15 (RBM15). Insulin like growth factor 2 mRNA binding protein 1 (IGF2BP1) was identified as the m(6)A reader protein of UBA6-AS1-RBM15-mediated m(6)A modification of UBA6 mRNA, which enhanced the stability of UBA6 mRNA. Functionally, UBA6-AS1 suppressed the proliferation, migration and invasion of OC cells via UBA6. Moreover, UBA6-AS1 positively correlated with UBA6 expression in OC tissues. Downregulation of UBA6-AS1 or UBA6 expression indicated poor. Collectively, we have identified a tumor-suppressive lncRNA that regulates its target mRNA via a m(6)A mechanism, highlighting the role that lncRNAs can play in OC progression.