4.5 Article

LncRNA CBR3-AS1 promotes osteosarcoma progression through the network of miR-140-5p/ DDX54-NUCKS1-mTOR signaling pathway

Journal

MOLECULAR THERAPY-ONCOLYTICS
Volume 25, Issue -, Pages 189-200

Publisher

CELL PRESS
DOI: 10.1016/j.omto.2022.03.001

Keywords

-

Ask authors/readers for more resources

The study found that CBR3-AS1 is highly expressed in osteosarcoma cells and promotes the stemness and EMT of these cells, as well as tumor growth.
Long noncoding RNA (lncRNA) CBR3-AS1 (termed as CBR3AS1) has been reported to be upregulated in several cancers including osteosarcoma. Its positive impact on the proliferation, migration, and invasion of osteosarcoma cells has been unveiled; nevertheless, whether it also affects the stemness and epithelial-mesenchymal transition (EMT) of osteosarcoma cells is unclear. The purpose for this study was to explore the effects of CBR3-AS1 on the stemness and EMT of osteosarcoma cells as well as its underlying mechanism. qRT-PCR and western blot were applied to detect target gene expression. Function assays were conducted to evaluate the effect of genes on the stemness and EMT of osteosarcoma cells. Mechanism assays were done to verify the association among different genes. In vivo assays were also performed. The obtained data showed that CBR3-AS1 demonstrated a high expression in osteosarcoma cells. CBR3-AS1 could promote stemness and EMT of osteosarcoma cells as well as osteosarcoma tumor growth. Mechanically, CBR3-AS1 sponged miR-140-5p and recruited DDX54 to upregulate NUCKS1, thus activating the mTOR stemness and EMT of osteosarcoma cells. In summary, this study reveals that CBR3-AS1 exerts an oncogenic role in osteosarcoma through modulating the network of the miR-1405p/DDX54-NUCKS1-mTOR signaling pathway.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.5
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available