ARID3A-mediated modulation of TP73 and TP73-AS1 in osteosarcoma cells
Yükleniyor...
Dosyalar
Tarih
2020
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Elsevier Inc
Erişim Hakkı
info:eu-repo/semantics/closedAccess
Özet
Osteosarcoma is the most common primary malignancy arising from bone. Increasing mass of indications suggest that long non-coding RNAs (lncRNAs) play crucial roles in the development of progressions of human cancers including osteosarcoma. Although several lncRNAs have shown to be involved in the molecular pathogenesis of osteosarcoma, identification of novel lncRNAs involved in the osteosarcoma pathobiology remained muchly elusive. Besides, ARID3A is a member of ARID family of DNA binding proteins. ARID3A was also implicated in osteosarcoma pathogenesis. Accordingly, in the present study, we mechanistically investigated the effect of ARID3A on the expression of TP73 and TP73-AS1 in osteosarcoma cells and to determine the relationship between them. For the overexpression of ARID3A in U2-OS cells, pER_xpress_ARID3A expression vector and for the silencing of ARID3A, ARID3A-spesific siRNA was used. Expression levels of ARID3A, TP73 and TP73-AS1 genes were determined by qPCR method. As a result, expression levels of TP73-AS1 were well-correlated with the ARID3A expression levels whereas TP73 expression levels were not well-correlated with ARID3A. In conclusion, our results indicate that ARID3A might be involved in the regulation of TP73-AS1 in osteosarcoma. To our knowledge, this is the first study revealing the role of ARID3A in the regulation of TP73 and TP73-AS1 genes. © 2020 Elsevier Inc.
Açıklama
Anahtar Kelimeler
ARID3A, lncRNA, non-coding RNA, Osteosarcoma, TP73, TP73-AS1, AT rich interaction domain 3a protein, complementary RNA, DNA binding protein, small interfering RNA, tumor protein p73, tumor protein p73 antisense RNA 1, unclassified drug, Article, controlled study, gene overexpression, gene silencing, osteosarcoma cell, polymerase chain reaction, priority journal, protein expression level, regulatory mechanism, U2OS cell line
Kaynak
Gene Reports
WoS Q Değeri
N/A
Scopus Q Değeri
Q4
Cilt
20
