B-Myb regulates snail expression to promote epithelial-to-mesenchymal transition and invasion of breast cancer cell

2014 ◽  
Vol 32 (1) ◽  
Author(s):  
Deyou Tao ◽  
Yihong Pan ◽  
Guobin Jiang ◽  
Hongsheng Lu ◽  
Song Zheng ◽  
...  
2020 ◽  
Vol 19 ◽  
pp. 153303382097967
Author(s):  
Jin Zhang ◽  
Nan Shao ◽  
Xiaoyu Yang ◽  
Chuanbo Xie ◽  
Yawei Shi ◽  
...  

The microRNA-200 (miR-200) family has been reported to be vital for the inhibition of epithelial-to-mesenchymal transition (EMT) in tumor cells. The miR-200 family represents a complex multi-factorial regulatory network which has not been well described in breast cancer. This study aimed to clarify the underlying regulatory association between IL-8 and miR-200 family in the process of EMT in breast cancer cell. In estrogen-receptor (ER) positive breast cancer cell line MCF-7, IL-8 overexpression cells were performed by lentivirus transfection as endogenous regulation with additional exogenous IL-8 stimulation. Transient overexpressions of miR-200 family were performed after endogenous or exogenous IL-8 overexpression in MCF-7 cells. IL-8 knockdown cells were constructed via siRNA and shRNA transfection in triple negative breast cancer cell line MDA-MB-231. N-cadherin, vimentin and ZEB2 were down-regulated and E-cadherin was up-regulated in IL-8 knockdown group compared with control group. On the other hand, N-cadherin, vimentin and ZEB2 were up-regulated and E-cadherin was down-regulated in IL-8 overexpression group compared with control group. This indicated IL-8 promotes EMT in breast cancer cells. Transwell assay showed that IL-8 increased the migration and invasiveness of tumor cells. Furthermore, we performed transient overexpression of miR-200 family after endogenous or exogenous IL-8 overexpression in MCF-7 cells, which showed that the miR-200 family could inhibit EMT induced by IL-8. IL-8 promoted EMT via downregulation of miR-200 family expression in breast cancer cells and increases tumor cell migration and invasion.


2021 ◽  
Vol 16 (10) ◽  
pp. 13-18
Author(s):  
Tehrani Azadeh Aghvami ◽  
Saeid Latifi-Navid ◽  
Saber Zahri ◽  
Mohsen Sagha

Bone morphogenetic protein (BMP) signaling is known as one of the most important pathways in breast cancer tumorigenesis. This triggers the epithelial to mesenchymal transition (EMT) in metastatic cells and consequently the migrating cells become invasive and noggin, a BMP antagonist prevents it. So, the present study aimed to optimize Noggin transfection into MCF-7 as a breast cancer cell line. Following DH5α bacterial cell culturing and pCMV3- Nog-GFPSpark transformation, the resulted plasmid was extracted, purified and finally transfected into MCF-7 at different voltages (100-230V), resistances (1000 and ∞ Ω) and capacitances (25-75μF) using the electroporation system with various concentrations of plasmid (between 30 and 100μg/ml). As a result, we found that noggin has a better transfection into MCF- 7 in 230V, 50μF, 1000 Ωof electroporator. At 80μg/ml concentration of plasmid, the cell expressing GFP also represented the noggin expression.


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