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MiR-214-3p regulates the viability, invasion, migration and EMT of TNBC cells by targeting ST6GAL1.
Cytotechnology ( IF 2.0 ) Pub Date : 2019-11-11 , DOI: 10.1007/s10616-019-00352-z
Yun Tao 1 , Zhijing Zhao 2 , Junfeng Ma 2 , Liying Dong 2 , Ying Liang 2 , Siqi Li 2 , Ying Mao 2 , Yan Li 2 , Yi Zhang 2
Affiliation  

MiR-214-3p is concerned with the outcomes of various tumors, such as liver cancer, bladder cancer, etc. However, the role and target of miR-214-3p in triple negative breast cancer (TNBC) is not fully understood. This study took this as the entry point, with a view to find a potential target for TNBC. The expressions of miR-214-3p in TNBC tissues and cell lines were detected, and the effects of miR-214-3p inhibitor on the viability, migration, invasion and epithelial mesenchymal transition (EMT) of TNBC cells were further analyzed. The potential target of miR-214-3p were predicted and verified, as well as the effects of target silencing on the TNBC cells were also measured. MiR-214-3p was abnormally elevated in both TNBC tissues and cell lines, especially in MDA-MB-468 cells. Low-expression of miR-214-3p restrained the survival, migration, invasion and EMT of TNBC cells. ST6GAL1 was the target gene of miR-214-3p, and its expression level increased with the low-expression of miR-214-3p. ST6GAL1 expression was abnormally reduced in both TNBC tissues and cell lines. The silence of ST6GAL1 promoted the viability, migration, invasion and EMT of TNBC cells, which could be reversed by miR-214-3p inhibitor. The down-regulation of miR-214-3p could suppress the viability, migration, invasion and EMT of TNBC cells though targeting ST6GAL1, which might be a potential target for future treatment of TNBC. Up-regulation of miR-214-3p could promote the EMT of non-TNBC cells.

中文翻译:

MiR-214-3p通过靶向ST6GAL1来调节TNBC细胞的活力,侵袭,迁移和EMT。

MiR-214-3p与各种肿瘤的预后有关,例如肝癌,膀胱癌等。但是,miR-214-3p在三阴性乳腺癌(TNBC)中的作用和靶标尚不完全清楚。这项研究以此为切入点,以期寻找TNBC的潜在目标。检测miR-214-3p在TNBC组织和细胞系中的表达,并进一步分析miR-214-3p抑制剂对TNBC细胞活力,迁移,侵袭和上皮间充质转化(EMT)的影响。预测并验证了miR-214-3p的潜在靶标,还测量了靶标沉默对TNBC细胞的影响。在TNBC组织和细胞系中,特别是在MDA-MB-468细胞中,MiR-214-3p异常升高。miR-214-3p的低表达抑制了存活,迁移,TNBC细胞的侵袭和EMT。ST6GAL1是miR-214-3p的靶基因,其表达水平随着miR-214-3p的低表达而增加。TNBC组织和细胞系中ST6GAL1表达均异常降低。ST6GAL1的沉默促进了TNBC细胞的活力,迁移,侵袭和EMT,而miR-214-3p抑制剂可以逆转这种作用。通过靶向ST6GAL1,miR-214-3p的下调可以抑制TNBC细胞的活力,迁移,侵袭和EMT,这可能是将来治疗TNBC的潜在目标。miR-214-3p的上调可以促进非TNBC细胞的EMT。ST6GAL1的沉默促进了TNBC细胞的活力,迁移,侵袭和EMT,而miR-214-3p抑制剂可以逆转这种作用。通过靶向ST6GAL1,miR-214-3p的下调可以抑制TNBC细胞的活力,迁移,侵袭和EMT,这可能是将来治疗TNBC的潜在目标。miR-214-3p的上调可以促进非TNBC细胞的EMT。ST6GAL1的沉默促进了TNBC细胞的活力,迁移,侵袭和EMT,而miR-214-3p抑制剂可以逆转这种作用。通过靶向ST6GAL1,miR-214-3p的下调可以抑制TNBC细胞的活力,迁移,侵袭和EMT,这可能是将来治疗TNBC的潜在目标。miR-214-3p的上调可以促进非TNBC细胞的EMT。
更新日期:2019-11-01
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