LncRNA BBOX1‐AS1 targets miR‐361‐3p/COL1A1 axis to drive the progression of oesophageal carcinoma

• Published in: European journal of clinical investigation Vol. 53; no. 4; pp. e13929 - n/a
• Main Authors: Ma, Ruidong, Lu, Yuhai, He, Xiaoping, Zeng, Xiaofei
• Format: Journal Article
• Language: English
• Published: England Blackwell Publishing Ltd 01.04.2023
• Subjects: 3' Untranslated regions; Apoptosis; BBOX1‐AS1; Blotting, Western; Cancer; Caspase; Cell Line, Tumor; Cell migration; Cell Movement; Cell Proliferation; Cell viability; Cholecystokinin; COL1A1; Collagen (type I); Esophageal cancer; Esophageal Neoplasms; Gene Expression Regulation, Neoplastic; Humans; In vivo methods and tests; Malignancy; MicroRNAs; miR‐361‐3p; Non-coding RNA; oesophageal carcinoma; Phenotypes; RNA, Long Noncoding; Tumors; Western blotting; COL1A1; oesophageal carcinoma; BBOX1-AS1; miR-361-3p
• ISSN: 0014-2972; 1365-2362
• DOI: 10.1111/eci.13929

Background Oesophageal 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. Methods In 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. Results BBOX1‐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. Conclusion BBOX1‐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.