Regulation of lamellipodia formation and cell invasion by CLIP-170 in invasive human breast cancer cells

2008 ◽  
Vol 368 (2) ◽  
pp. 199-204 ◽  
Author(s):  
Katsuo Suzuki ◽  
Kazuhide Takahashi
Endocrinology ◽  
2012 ◽  
Vol 153 (2) ◽  
pp. 554-563 ◽  
Author(s):  
Su-Ryun Kim ◽  
Hyun-Joo Park ◽  
Yun-Hee Bae ◽  
Soon-Cheol Ahn ◽  
Hee-Jun Wee ◽  
...  

Obesity is frequently associated with breast cancer. Such associations are possibly mediated by adipokines. Visfatin, an adipokine, has recently been shown to be related to the development and progression of breast cancer. Therefore, the down-regulation of visfatin may be a novel strategy for breast cancer therapy. Curcumin has anticancer activities by modulating multiple signaling pathways and genes. The purpose of this study was to investigate whether visfatin gene expression is affected by curcumin in human breast cancer cells and to characterize the functional role of visfatin in breast cancer. We found that the mRNA and protein levels of visfatin were down-regulated by curcumin in MDA-MB-231, MDA-MB-468, and MCF-7 breast cancer cells, along with decreased activity of constitutive nuclear factor (NF)-κB. We confirmed the repressive effect of curcumin on visfatin transcription by performing a visfatin promoter-driven reporter assay and identified two putative NF-κB-binding sites on visfatin promoter that are important for this effect. EMSA and chromatin immunoprecipitation analysis indicated the binding of p65 to the visfatin promoter, which was effectively blocked by curcumin. Enforced expression of p65 protein increased visfatin promoter activity, whereas blocking NF-κB signaling suppressed visfatin gene expression. Visfatin could enhance the invasion of MDA-MB-231 cells and also attenuate curcumin-induced inhibition of cell invasion; on the other hand, visfatin knockdown by small interfering RNA led to the reduction of cell invasion. Our data demonstrate, for the first time, that curcumin down-regulates visfatin gene expression in human breast cancer cells by a mechanism that is, at least in part, NF-κB dependent and suggest that visfatin may contribute to breast cancer cell invasion and link obesity to breast cancer development and progression.


Molecules ◽  
2008 ◽  
Vol 13 (12) ◽  
pp. 2975-2985 ◽  
Author(s):  
Sangmin Kim ◽  
Jae Hyuck Choi ◽  
Jong Bin Kim ◽  
Seok Jin Nam ◽  
Jung-Hyun Yang ◽  
...  

2014 ◽  
Vol 9 (6) ◽  
pp. 647-658 ◽  
Author(s):  
Urszula Lewandowska ◽  
Katarzyna Owczarek ◽  
Karolina Szewczyk ◽  
Dorota Sosnowska ◽  
Maria Koziołkiewicz ◽  
...  

AbstractThis study examines some of the biological activities of an evening primrose flavanol preparation (EPFP) against non-invasive human breast cancer cells (MCF-7). The results are compared with those obtained for highly invasive human breast cancer cells (MDAMB-231). The results show, for the first time, that EPFP reduces MCF-7 cell number, IC50 = 75 µM gallic acid equivalents/GAE for 72 h incubation, and reduces migration to 52% of the control value at 100 µM L−1 GAE. EPFP caused favorable changes in Bcl-2/Bax mRNA ratio, which rendered MCF-7 cells more sensitive to apoptosis: the number of apoptotic cells increased 2.2-fold vs. control at 100 µM GAE. Furthermore, 100 µ M L−1 GAE EPFP caused a 1.8-fold reduction in the activity of metalloproteinase-9 (MMP-9) secreted to the culture medium by MCF-7 cells. Moreover, EPFP suppressed the expression of selected genes of matrix metalloproteinases (MMPs), a proliferation marker (Ki67), and vascular endothelial growth factor (VEGF). In conclusion, the results of this study suggest that EPFP may exhibit proapoptotic, antiproliferative, antimigratory, and antimetastatic potential towards both selected human breast cancer cell lines, which is more pronounced in the case of the highly invasive MDA-MB-231 cells.


Cell Cycle ◽  
2007 ◽  
Vol 6 (16) ◽  
pp. 2038-2042 ◽  
Author(s):  
Amber Yasmeen ◽  
Tarek A. Bismar ◽  
Mustapha Kandouz ◽  
William D. Foulkes ◽  
Pierre-Yves Desprez ◽  
...  

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