Low-level lasers on microRNA and uncoupling protein 2 mRNA levels in human breast cancer cells

Laser Physics ◽  
2017 ◽  
Vol 27 (6) ◽  
pp. 065601 ◽  
Author(s):  
K S Canuto ◽  
A F Teixeira ◽  
J A Rodrigues ◽  
F Paoli ◽  
E M Nogueira ◽  
...  
2009 ◽  
Vol 37 (01) ◽  
pp. 159-167 ◽  
Author(s):  
Mi-Kyung Park ◽  
Hyeok-Yi Kwon ◽  
Woong-Shick Ahn ◽  
Sumi Bae ◽  
Mee-Ra Rhyu ◽  
...  

We studied the estrogenic activity and cellular effect of wild yam extract in MCF-7 human breast cancer cells. The extract increased the activity of the progesterone receptor and pS2 genes at the mRNA levels in human breast cancer MCF-7 cells, although the effects were not as prominent as those of 17β-estradiol (E2). Western blot analysis showed that the level of estrogen receptor α protein was down-regulated after treatment with E2 or wild yam extract. Wild yam extract also inhibited proliferation of MCF-7 cells. These data indicate that wild yam extract acts as a weak phytoestrogen and protects against proliferation in human breast carcinoma MCF-7 cells.


1989 ◽  
Vol 3 (4) ◽  
pp. 694-702 ◽  
Author(s):  
Jacques Simard ◽  
Anne Catherine Hatton ◽  
Claude Labrief ◽  
Sophie Dauvois ◽  
Hui Fen Zhao ◽  
...  

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. e13578-e13578 ◽  
Author(s):  
Burcu Cakar ◽  
Pinar Gursoy ◽  
Harika Atmaca ◽  
Asli Kisim ◽  
Emir Bozkurt ◽  
...  

e13578 Background: Paclitaxel, a microtubule stabilizing agent, has been a standard of care for breast cancer. AT-101, is an -/- enantiomer of gossypol, inhibits the Bcl-2 family proteins which contain BH3 domain. We reported previously that Paclitaxel in combination with AT-101 showed strong synergistic cytotoxic and apoptotic effects in human breast cancer cells. In this study, to elucidate the molecular mechanisms involved in the apoptotic effect of AT-101/Paclitaxel combination treatment in breast cancer cells, we investigated the possible roles of anti-apoptotic Bcl-2, Bcl-XL and Mcl-1 proteins which contain BH3 domain. Involvement of caspase 3 and 7 activation was also investigated. Methods: Human breast cancer cells were treated with increasing concentrations of drugs alone or with the synergistic combination doses of AT-101 and Paclitaxel. Cell Death Detection Elisa Plus Kit (Roche) was used to detect apoptosis. Caspase 3/7 activity was evaluated by Caspase-Glo 3/7 (Promega, Madison, WI) kit. Changes in the mRNA levels of Bcl-2, Bcl-XL and Mcl-1 genes were evaluated by qRT-PCR. Expression levels of these proteins were also investigated by Western blot analysis. Results: Combined treatment was shown to have strong synergistic apoptotic effects in MCF-7 and MDA- MB-231 human breast cancer cells. mRNA levels of Bcl-2, Bcl-XL and Mcl-1 molecules were reduced by the combination treatment in both cell lines. In parallel with mRNA levels, Bcl-2, Bcl-XL and Mcl-1 protein levels were significantly reduced after this novel drug combination. Combined treatment also induced caspase 3/7 activation in breast cancer cells. Conclusions: These preliminary data suggest that anti-apoptotic proteins such as Bcl-2, Bcl-XL and Mcl-1 may play important role in the underlying mechanistic rationale of apoptotic effect of AT-101/paclitaxel combination, while pro-apoptotic Bcl-2 related genes (Caspase-3 and Caspase-7) also seem to regulate this synergistic interaction.


1991 ◽  
Vol 7 (2) ◽  
pp. 105-112 ◽  
Author(s):  
L. Dejardin ◽  
R. Gol-Winkler ◽  
J. Collette ◽  
C. Delvenne ◽  
I. Carlisi ◽  
...  

ABSTRACT Oestradiol-17β and tamoxifen regulate the synthesis of a gross cystic disease fluid protein (GCDFP-15) in T47D human breast cancer cells. Dose-response curves of GCDFP-15 mRNA contents and GCDFP-15 levels in culture media and cells versus hormone or antihormone concentration have been established. Production of GCDFP-15 was increased by oestradiol-17β, tamoxifen and 4-OH tamoxifen. The effect of tamoxifen and 4-OH tamoxifen was greater than the effect of oestradiol-17β. Moreover, oestradiol-17β and 4-OH tamoxifen acted synergystically in enhancing GCDFP-15 release. The strong oestrogenic effect of the antioestrogen tamoxifen in regulating GCDFP-15 may reflect an unusual interaction between the tamoxifen-oestrogen receptor complex and the DNA oestrogen-responsive elements. As oestrogen control of GCDFP-15 depends also on the cell line studied, investigation of GCDFP-15 could extend our knowledge of the possible mechanism of action of oestrogens or antioestrogens.


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