Dysfunction of the ST7-AS1/miR-301b-3p/BTG1 ceRNA network promotes immune escape of triple-negative breast cancer

• Published in: International immunopharmacology 2023-03, Vol.116, p.109805, Article 109805
• Main Authors: Li, Yong, Xin, Wenge, Liu, Fang, Li, Fengjuan, Yang, Chengmin, Liu, Changmin, Liu, Jiaxin
• Format: Article
• Language: English
• Subjects: BTG1; ceRNA network; Immune escape; Long noncoding RNA; microRNA-301b-3p; ST7-AS1; Triple-negative breast cancer; Whole transcriptome sequencing
• ISSN: 1567-5769; 1878-1705
• DOI: 10.1016/j.intimp.2023.109805

•1. This study is based on whole transcriptome sequencing and differential analysis of TCGA data.•2. Prognostic risk model based on 18 ceRNA network-related genes predicts TNBC prognosis.•3. Expression of ST7-AS1 and BTG1 is down-regulated in tumors of TNBC.•4. miR-301b-3p expression is up-regulated in TNBC tumors of TNBC.•5. ST7-AS1/miR-301b-3p/BTG1 is the key ceRNA regulatory network in immune escape of TNBC. Functional interactions in ceRNA regulatory networks coordinate a wide array of biologic processes and, contribute to cancer pathogenesis when perturbed. The current study was performed to explore the role of a newly constructed lncRNA-miRNA-mRNA ceRNA network in immune escape in triple-negative breast cancer (TNBC). We constructed an orthotopic tumor model of TNBC in nude mice, where tumor tissue was collected for whole transcriptome sequencing. The ceRNA regulatory network was constructed according to the data from TNBC-related whole transcriptome sequencing and differential analysis of TCGA database. Accordingly, a ceRNA regulatory network ST7-AS1/miR-301b-3p/BTG1 related to the prognosis of TNBC patients was identified. The in vivo experiments further confirmed that the expression of ST7-AS1 and BTG1 was down-regulated, but miR-301b-3p expression was up-regulated in orthotopic transplanted tumor tissues of mice. Furthermore, ST7-AS1 might upregulate BTG1 expression by sequestering miR-301b-3p, which promoted the activity of CD8 + T cells, thus inhibiting the development of TNBC. Taken together, our study emphasized that ST7-AS1 might promote BTG1 expression by competitively binding to miR-301b-3p, thereby restricting immune escape in TNBC.