LncRNA BBOX1-AS1 targets miR-361-3p/COL1A1 axis to drive the progression of esophageal carcinoma.

BACKGROUND
Esophageal carcinoma (EC) is one of the types of prevalent malignant cancer in the globe. Many researchers reported the vital role played by long-coding RNAs in EC. In current research, we investigated the mechanisms of action of lncRNA BBOX1-AS1 in EC progression.


METHODS
In EC tissues as well as EC cells, the expression levels of miR-361-3p along with COL1A1 and BBOX1-AS1 were detected through RT-qPCR or western blotting. MiR-361-3p interactions with BBOX1-AS1 or COL1A1 were verified through Luciferase reporter and RIP tests. Loss-of-function combined with caspase-3 activity, CCK-8, and Transwell assays were performed to investigate cell apoptosis, proliferation and migration, respectively. Knockdown of BBOX1-AS1 was used for evaluating BBOX1-AS1 effects on tumor development in vivo.


RESULTS
BBOX1-AS1 was remarkably elevated in EC tissues as well as cells. In addition, silencing of BBOX1-AS1 attenuated the cell viability, cell migration, and enhanced cell apoptosis of EC, as well as suppressed EC tumor formation in vivo. Moreover, BBOX1-AS1 was found to be a sponge of miR-361-3p which down-regulated miR-361-3p expression. MiR-361-3p inhibitor rescued the anti-tumor effect of BBOX1-AS1 knockdown on the progression of EC. Furthermore, we discovered that miR-361-3p specially bound to COL1A1 3'UTR and downregulated COL1A1, and COL1A1 reduction declined the promoting effect of silencing miR-361-3p on EC cell malignant phenotypes.


CONCLUSION
BBOX1-AS1 facilitated the EC development and malignancy via miR-361-3p/COL1A1 axis, indicating BBOX1-AS1 could be a novel therapy target on the diagnostic of EC.