scholarly journals Ani-survivin DNAzymes Inhibit Cell Proliferation and Migration in Breast Cancer Cell Line MCF-7

2012 ◽  
Vol 13 (12) ◽  
pp. 6233-6237 ◽  
Author(s):  
Min Zhang ◽  
Yi-Fu Sun ◽  
Su Luo
2011 ◽  
Vol 131 (2) ◽  
pp. 276-286 ◽  
Author(s):  
Philip J. Medeiros ◽  
Baraa K. Al-Khazraji ◽  
Nicole M. Novielli ◽  
Lynne M. Postovit ◽  
Ann F. Chambers ◽  
...  

Drug Research ◽  
2020 ◽  
Vol 70 (10) ◽  
pp. 478-483
Author(s):  
Hamed Esmaeil Lashgarian ◽  
Vahid Adamii ◽  
Vajihe Ghorbanzadeh ◽  
Leila Chodari ◽  
Fayze Kamali ◽  
...  

Abstract Background Triple negative breast cancer is the most invasive breast cancer subtype and possesses poor prognosis and survival. Rho GTPase famil, especially Rac1 participates in a number of signaling events in cells with crucial roles in malignancy, migration and invasion of tumor cells. Silibinin, a flavonoid antioxidant from milk thistle has attracted attention in the recent decades for chemoprevention and chemotherapy of tumor cells. In this study, the effect of silibinin on the migration capacity of MDA-MB-231 cells, a highly metastatic human breast cancer cell line was investigated by evaluation of Rac1 expression. Method MTT wound healing and transwell assays were performed to evaluate the effects of silibinin on proliferation and migration of MDA-MB-231 cells. In addition, the influence of the silibinin on the expression of Rac1mRNAs was assessed by RT-PCR. Results Results indicated significant dose-dependent inhibitory effect of silibinin on proliferation and migration of MDA-MB-231 cells. It significantly inhibited the expression of Rac1 mRNA. Conclusion In conclusion, the results demonstrate that the silibinin can be used as an experimental therapeutic for the management of TNBC metastatic cancer.


2016 ◽  
Vol 90 ◽  
pp. 45-54 ◽  
Author(s):  
Filipa S. Reis ◽  
Diana Sousa ◽  
Lillian Barros ◽  
Anabela Martins ◽  
Patricia Morales ◽  
...  

2015 ◽  
Vol 35 (24) ◽  
pp. 4170-4184 ◽  
Author(s):  
Yuji Tanaka ◽  
Hirohisa Yano ◽  
Sachiko Ogasawara ◽  
Sho-ichi Yoshioka ◽  
Hiromi Imamura ◽  
...  

Environmental conditions control rRNA transcription. Previously, we found that serum and glucose deprivation induces KDM2A-mediated H3K36me2 demethylation in the rRNA gene (rDNA) promoter and reduces rRNA transcription in the human breast cancer cell line MCF-7. However, the molecular mechanism and biological significance are still unclear. In the present study, we found that glucose starvation alone induced the KDM2A-dependent reduction of rRNA transcription. The treatment of cells with 2-deoxy-d-glucose, an inhibitor of glycolysis, reduced rRNA transcription and H3K36me2 in the rDNA promoter, both of which were completely dependent on KDM2A in low concentrations of 2-deoxy-d-glucose, that is, mild starvation conditions. The mild starvation induced these KDM2A activities through AMP-activated kinase (AMPK) but did not affect another AMPK effector of rRNA transcription, TIF-IA. In the triple-negative breast cancer cell line MDA-MB-231, the mild starvation also reduced rRNA transcription in a KDM2A-dependent manner. We detected KDM2A in breast cancer tissues irrespective of their estrogen receptor, progesterone receptor, and HER2 status, including triple-negative cancer tissues. In both MCF-7 and MDA-MB-231 cells, mild starvation reduced cell proliferation, and KDM2A knockdown suppressed the reduction of cell proliferation. These results suggest that under mild glucose starvation AMPK induces KDM2A-dependent reduction of rRNA transcription to control cell proliferation.


2007 ◽  
Vol 14 (2) ◽  
pp. 325-335 ◽  
Author(s):  
Frauke Döll ◽  
Josef Pfeilschifter ◽  
Andrea Huwiler

Sphingosine kinases (SK) catalyze the formation of sphingosine-1-phosphate (S1P) which plays a crucial role in cell growth and survival. Here, we show that prolactin (PRL) biphasically activates the SK-1, but not the SK-2 subtype, in the breast adenocarcinoma cell-line MCF7. A first peak occurs after minutes of stimulation and is followed by a second delayed activation after hours of stimulation. A similar biphasic effect on SK-1 activity is seen for 17β-estradiol (E2). The delayed activation of SK-1 derives from an upregulated mRNA and protein expression and is due to increased SK-1 promoter activity and mechanistically involves STAT5 activation as well as protein kinase C and the classical mitogen-activated protein kinases. Furthermore, glucocorticoids also block both hormone-induced SK-1 expression and activity. Functionally, long-term stimulation of MCF7 cells with PRL or E2 is well known to trigger increased cell proliferation and migration. Both hormone-induced cell responses critically involve SK-1 activation since the depletion of SK-1, but not SK-2, by siRNA transfection abolishes the hormone-induced cell proliferation and migration. In summary, our data show that PRL and E2 cause a pronounced delayed SK-1 activation which is due to increased gene transcription, and critically determines the capability of cells to grow and move. Thus, the SK-1 may represent a novel attractive target for anti-tumor therapy.


2010 ◽  
Vol 192 (2) ◽  
pp. 195-205 ◽  
Author(s):  
María Alejandra García ◽  
Delfina Peña ◽  
Laura Álvarez ◽  
Claudia Cocca ◽  
Carolina Pontillo ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document