DNA polymerase iota (Pol ι) promotes the migration and invasion of breast cancer cell via EGFR-ERK-mediated epithelial to mesenchymal transition

2019 ◽  
Vol 24 (3) ◽  
pp. 363-370 ◽  
Author(s):  
Shitao Zou ◽  
Yan Xu ◽  
Xingxing Chen ◽  
Chao He ◽  
Aidi Gao ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cell ◽  
Dna Polymerase ◽  
Breast Cancer Cell ◽  
Epithelial To Mesenchymal Transition ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Dna Polymerase Iota

scholarly journals Interleukin-8 Promotes Epithelial-to-Mesenchymal Transition via Downregulation of Mir-200 Family in Breast Cancer Cells

2020 ◽  
Vol 19 ◽  
pp. 153303382097967
Author(s):  
Jin Zhang ◽  
Nan Shao ◽  
Xiaoyu Yang ◽  
Chuanbo Xie ◽  
Yawei Shi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Cancer Cell Line ◽  
Control Group ◽  
Mesenchymal Transition ◽  
Mcf 7

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.

scholarly journals ppGalNAc-T4-catalyzed O-Glycosylation of TGF-β type Ⅱ receptor regulates breast cancer cells metastasis

2020 ◽  
pp. jbc.RA120.016345
Author(s):  
Qiong Wu ◽  
Cheng Zhang ◽  
Keren Zhang ◽  
Qiushi Chen ◽  
Sijin Wu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Transforming Growth Factor Beta ◽  
Breast Cancer Cells ◽  
Transforming Growth Factor ◽  
Migration And Invasion ◽  
Breast Cancer Cell Lines ◽  
Mesenchymal Transition

GalNAc-type O-glycosylation, initially catalyzed by polypeptide N-acetylgalactosaminyltransferases (ppGalNAc-Ts), is one of the most abundant and complex post-translational modifications of proteins. Emerging evidence has proven that aberrant ppGalNAc-Ts are involved in malignant tumor transformation. However, the exact molecular functions of ppGalNAc-Ts are still unclear. Here, the role of one isoform, ppGalNAc-T4, in breast cancer cell lines was investigated. The expression of ppGalNAc-T4 was found to be negatively associated with migration of breast cancer cells. Loss-of function studies revealed that ppGalNAc-T4 attenuated the migration and invasion of breast cancer cells by inhibiting the epithelial-mesenchymal transition (EMT) process. Correspondingly, transforming growth factor beta (TGF-β) signaling, which is the upstream pathway of EMT, was impaired by ppGalNAc-T4 expression. ppGalNAc-T4 knock-out decreased O-GalNAc modification of TGF-β type Ⅰ and Ⅱ receptor (TβR Ⅰ and Ⅱ) and led to the elevation of TGF-β receptor dimerization and activity. Importantly, a peptide from TβR Ⅱ was first identified as the naked peptide substrate of ppGalNAc-T4 with a higher affinity than ppGalNAc-T2. Further, Ser31, corresponding to the extracellular domain of TβR Ⅱ, was identified as the O-GalNAcylation site upon in vitro glycosylation by ppGalNAc-T4. The O-GalNAc-deficient S31A mutation enhanced TGF-β signaling activity and EMT in breast cancer cells. Together, these results identified a novel mechanism of ppGalNAc-T4-catalyzed TGF-β receptors O-GalNAcylation that suppresses breast cancer cell migration and invasion via the EMT process. Targeting ppGalNAc-T4 may be a potential therapeutic strategy for breast cancer treatment.

Optimization of pCMV3-Nog-C-GFPSpark Electro-transfection in MCF-7, a Breast Cancer Cell Line

2021 ◽  
Vol 16 (10) ◽  
pp. 13-18
Author(s):  
Tehrani Azadeh Aghvami ◽  
Saeid Latifi-Navid ◽  
Saber Zahri ◽  
Mohsen Sagha
Keyword(s):  
Breast Cancer ◽  
Cell Line ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cell Line ◽  
Epithelial To Mesenchymal Transition ◽  
Cancer Cell Line ◽  
Bmp Signaling ◽  
Mesenchymal Transition ◽  
Mcf 7

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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