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

被引:1
|
作者
Li, Yong [1 ,2 ,3 ]
Xin, Wenge [3 ]
Liu, Fang [3 ]
Li, Fengjuan [4 ]
Yang, Chengmin [1 ,2 ]
Liu, Changmin [1 ,2 ,5 ]
Liu, Jiaxin [1 ]
机构
[1] Chinese Acad Med Sci & Peking Union Med Coll, Inst Blood Transfus, 26 Huacai Rd, Chengdu 610052, Peoples R China
[2] Tianjin Union Biotechnol Co LTD, Tianjin 300450, Peoples R China
[3] Tianjin Med Univ, Tianjin Med Univ Canc Inst & Hosp, Natl Clin Res Ctr Canc, Tianjins Clin Res Ctr Canc,Minist Educ,Intervent T, Tianjin 300060, Peoples R China
[4] Tiangong Univ, Sch Pharm, Dept Pharmaceut Engn, Tianjin 300387, Peoples R China
[5] Binzhou Med Univ Hosp, Dept Oncol, Binzhou 256603, Peoples R China
关键词
ceRNA network; Triple-negative breast cancer; Whole transcriptome sequencing; Long noncoding RNA; ST7-AS1; Immune escape; microRNA-301b-3p; BTG1; EXPRESSION; BTG1; CELLS; IDENTIFICATION; PATHOGENESIS;
D O I
10.1016/j.intimp.2023.109805
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
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页数:12
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