基因敲除
波形蛋白
细胞生长
癌症研究
MCF-7型
庆大霉素保护试验
MTT法
细胞培养
激酶
化学
HEK 293细胞
细胞
污渍
分子生物学
生物
细胞生物学
癌细胞
癌症
转移
免疫学
生物化学
人体乳房
遗传学
免疫组织化学
基因
作者
Jiao Tang,Xiaojing Zhang,Chunchun Chen,Binbin Wang,Yansong Chen,Hao Zhang,Mengxiang Qiao,Xianfu Liu,Wei Guo,Gongsheng Jin
标识
DOI:10.18388/abp.2020_6842
摘要
LncRNA MIR31HG is involved in many types of cancers, while its roles in breast cancer are still unknown. The current study aimed to explore the function of lncRNA MIR31HG in breast cancer and the underlying mechanisms. Stable expression cell lines were constructed by using lentivirus particles. MTT assay was used to determine cell viability. Wound healing and Transwell assay were used to determine cell migration and invasion, respectively. The changes in biomarkers were determined by using qPR-PCT and Western blotting, respectively. BALB/c nude mice were used to generate a xenograft mouse model. MIR31HG regulated cell proliferation, migration and invasion in MCF7 cells. Besides, MIR31HG regulated N-Cadherin, Vimentin, and E-Cadherin. MIR31HG positively regulated receptor-interacting serine-threonine kinase 4 (RIPK4), as supported by the fact that knockdown of MIR31HG suppressed RIPK4, and the knockdown of RIPK4 did not affect MIR31HG. Additionally, we found that RIPK4 regulated cell proliferation, migration and invasion in MCF7 cells. The changes in RIPK4 regulated N-Cadherin, Vimentin, and E-Cadherin. Consistently, in vivo studies showed that the knockdown of MIR31HG or RIPK4 reduced tumor size in xenograft animal models. The roles of lncRNA MIR31HG in breast cancer were associated with its regulatory effects against RIPK4.
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