• Eur. J. Clin. Invest. · Apr 2023

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

    • Ruidong Ma, Yuhai Lu, Xiaoping He, and Xiaofei Zeng.
    • Department of Cardiothoracic Surgery, First Affiliated Hospital of Chengdu Medical College, Chengdu, China.
    • Eur. J. Clin. Invest. 2023 Apr 1; 53 (4): e13929e13929.

    BackgroundOesophageal 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 the current research, we investigated the mechanisms of the action of lncRNA BBOX1-AS1 in EC progression.MethodsIn EC tissues and 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 was performed to investigate cell apoptosis, proliferation and migration, respectively. Knockdown of BBOX1-AS1 was used for evaluating BBOX1-AS1 effects on tumour development in vivo.ResultsBBOX1-AS1 was remarkably elevated in EC tissues and cells. In addition, the silencing of BBOX1-AS1 attenuated the cell viability, cell migration and enhanced cell apoptosis of EC, as well as suppressed EC tumour formation in vivo. Moreover, BBOX1-AS1 was found to be a sponge of miR-361-3p, which downregulated miR-361-3p expression. MiR-361-3p inhibitor rescued the anti-tumour 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.ConclusionBBOX1-AS1 facilitated the EC development and malignancy via miR-361-3p/COL1A1 axis, indicating BBOX1-AS1 could be a novel therapy target for the diagnostic of EC.© 2022 Stichting European Society for Clinical Investigation Journal Foundation. Published by John Wiley & Sons Ltd.

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