流浪汉
前列腺癌
生物
癌症研究
转基因小鼠
小RNA
转基因
前列腺
转移
癌症
体内
癌变
癌细胞
基因
遗传学
生物技术
生物化学
作者
Can Wang,Wenchao Li,Qiang Hu,Na Feng,Chunhui Liu,Naipeng Shi,Shuqiu Chen,Ming Chen,Han Guan,Zonghao You,Bin Xu
出处
期刊:Oncogene
[Springer Nature]
日期:2022-09-10
卷期号:41 (41): 4645-4657
被引量:4
标识
DOI:10.1038/s41388-022-02461-0
摘要
Although miR-7 suppresses the initiation and progression in cancers, little is known about its role in prostate cancer, especially in transgenic mouse models. In present study, we found that expression of miR-7, regulated by p53, was lower in prostate cancer tissues, and miR-7 overexpression significantly mitigated prostate cancer cells growth both in vitro, in organoids and in vivo regardless of p53 status. After we generated miR-7 overexpression transgenic mice and miR-7+/TRAMP mice, we found that transgenic overexpression of miR-7 in mice is safe and miR-7+/TRAMP mice have a preferred overall survival. Moreover, in vivo treatment of miR-7 inhibited subcutaneous tumour growth in mice and prolonged the survival of mice harboring prostate cancer lung metastasis when co-injection with PD-1 antibody. In addition, miR-7 downregulated glycolysis of prostate cancer cells by inhibiting several key pathways including HIF-1α, and subsequently remodeled acidic tumour microenvironment, PanKLa level and T cell infiltration. In summary, our findings highlighted a promising target for development of miRNA-based therapeutics for prostate cancer patients regardless of p53 status.
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