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1

FAK-independent regulation of prolidase activity and collagen biosynthesis in MCF-7 cells

100%
Surazynski A., Palka J.
Folia Histochemica et Cytobiologica. Supplement
|
2001
|
tom 39
|
nr 1
2

Proline analogue of melphalan as a prolidase-convertible pro-drug in breast cancer MCF-7 cells

75%
Chrzanowski K., Palka J.
Folia Histochemica et Cytobiologica. Supplement
|
2001
|
tom 39
|
nr 1
3

The interactions between SATB1 and F-actin are important for mechanisms of active cell death

63%
Grzanka D., Kowalczyk A. E., Izdebska M., Klimaszewska- -Wisniewska A., Gagat M.
Folia Histochemica et Cytobiologica
|
2015
|
tom 53
|
nr 2
4

The alterations in SATB1 and nuclear F-actin expression affect apoptotic response of the MCF-7 cells to geldanamycin

63%
Grzanka D., Izdebska M., Klimaszewska-Wisniewska A., Gagat M.
Folia Histochemica et Cytobiologica
|
2015
|
tom 53
|
nr 1
5
Content available remote

Cathepsins and BID are involved in the molecular switch between apoptosis and autophagy in breast cancer MCF-7 cells exposed to camptothecin

63%
Lamparska-Przybysz M., Gajkowska B., Motyl T.
Journal of Physiology and Pharmacology. Supplement
|
2005
|
tom 56
|
nr 3
159-179
The details of molecular switching points between apoptosis and autophagy in tumor cells have still not been fully elucidated. This study focused on the role of cathepsin B and its substrate, BID as molecular links between apoptosis and autophagy in human breast cancer MCF-7 cells exposed to camptothecin. Apoptosis occurred rapidly with a peak in 60 min after drug administration, whereas autophagy developed at a much slower rate with continuous progression during 24 h of cell exposure to the drug. CPT induced very rapid activation of cathepsin B. Inhibition of cathepsins by E64d prevented CPT-induced BAX and BID aggregation on mitochondria and reduced significantly reduced apoptotic cell number. The above effects were accompanied by an increase in autophagosome formation, measured by expression of MAP I LC3. BID knock down resulted in strong suppression of CPT-induced apoptosis and a shift of cell death towards autophagy, manifesting with an increase of Beclin 1 and MAP I LC3 cellular content.
6

Estrogen regulation and ion dependence of taurine uptake by MCF-7 human breast cancer cells

63%
Shennan D. B., Thomson J.
Cellular and Molecular Biology Letters
|
2007
|
tom 12
|
nr 3
It has been reported that estrogen receptor-positive MCF-7 cells express TauT, a Na+-dependent taurine transporter. However, there is a paucity of information relating to the characteristics of taurine transport in this human breast cancer cell line. Therefore, we have examined the characteristics and regulation of taurine uptake by MCF-7 cells. Taurine uptake by MCF-7 cells showed an absolute dependence upon extracellular Na+. Although taurine uptake was reduced in Cl- free medium a significant portion of taurine uptake persisted in the presence of NO3 -. Taurine uptake by MCF-7 cells was inhibited by extracellular β-alanine but not by L-alanine or L-leucine. 17β-estadiol increased taurine uptake by MCF-7 cells: the Vmax of influx was increased without affecting the Km. The effect of 17β-estradiol on taurine uptake by MCF-7 cells was dependent upon the presence of extracellular Na+. In contrast, 17β-estradiol had no significant effect on the kinetic parameters of taurine uptake by estrogen receptor-negative MDA-MB-231 cells. It appears that estrogen regulates taurine uptake by MCF-7 cells via TauT. In addition, Na+-dependent taurine uptake may not be strictly dependent upon extracellular Cl-.
7

The effect of Topotecan on oxidative stress in MCF-7 human breast cancer cell line

63%
Timur M., Akbas S. H., Ozben T.
Acta Biochimica Polonica
|
2005
|
tom 52
|
nr 4
Purpose. Topotecan, a semisynthetic water-soluble derivative of camptothecin exerts its cytotoxic effect by inhibiting topoisomerase I and causes double-strand DNA breaks which inhibit DNA function and ultimately lead to cell death. In previous studies it was shown that camptothecin causes ROS formation. The aim of this study was to investigate if Topotecan like camptotecin causes oxidative stress in MCF-7 human breast cancer cell line. Determining the oxidant effect of Topotecan may elucidate a possible alternative mechanism for its cytotoxicity. Experimental design. MCF-7 cells were cultured and exposed to Topotecan for 24 h at 37°C. The viability of the cells (% of control) was measured using the colorimetric 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. Lipid peroxidation (TBARS), protein oxidation (carbonyl content), sulfhydryl, glutathione (GSH) levels, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities were determined in MCF-7 cells with and without Topotecan incubation. Results. We found the IC50 concentration of Topotecan as 0.218 μM in MCF-7 cells. This concentration of Topotecan was used in the incubations of the cells. Our data indicated increased oxidative status, as revealed by increased lipid peroxidation and protein oxidation, and decreased GSH and sulfhydryl levels in MCF-7 cells exposed to Topotecan compared to control cells. In contrast, there was a slight increase in SOD and a significant increase in GPx and catalase activity in MCF-7 cells incubated with Topotecan compared to the control. Conclusions. These results support our hypothesis that Topotecan increases oxidative stress in MCF-7 cells.
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