Concentration Dependent Different Action of Tamoxifen on Membrane Fluidity

Kazancı, Nadide; Severcan, Feride

doi:10.1007/s10540-007-9050-3

Cited by 31 publications

(25 citation statements)

References 35 publications

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“…Assessments made through fluorescence polarization, DSC and turbidity are concurrent with the findings referred above, indicating that tamoxifen causes higher acyl chain disorder and, therefore, increased membrane fluidity in DMPC, DPPC and DSPC model membranes [97][98][99]. chains and present a weak cytotoxic activity [106].…”

Section: Studies Using Dsc and Langmuir Isotherms Demonstrated That Psupporting

confidence: 59%

Biophysics in cancer: The relevance of drug-membrane interaction studies

Alves

Ribeiro

Nunes

et al. 2016

Biochimica et Biophysica Acta (BBA) - Biomembranes

171

144

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Lipidomics has been proving that membrane lipids play a crucial role in several cell functions and are involved in several pathologies, including cancer. In fact, beyond a scaffold where proteins and other components are embedded, the cell membrane can also act as a barrier or a target for anticancer drugs. From this point of view, the development of new chemotherapeutic agents should also take into account the role of the membrane in their activity. This Review aims to highlight the importance of anticancer drug-membrane interactions as a powerful strategy to improve cancer therapy. Biophysical techniques emerge, therefore, as essential tools to unveil such interactions.

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Section: Studies Using Dsc and Langmuir Isotherms Demonstrated That Psupporting

confidence: 59%

Biophysics in cancer: The relevance of drug-membrane interaction studies

Alves

Ribeiro

Nunes

et al. 2016

Biochimica et Biophysica Acta (BBA) - Biomembranes

171

144

View full text Add to dashboard Cite

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“…Thus, tamoxifen at high doses (10 M) caused lysis (necrosis) of almost all cells within 24 h that cannot be prevented by estradiol . The cytotoxic action of tamoxifen may result from perturbations in membrane fluidity (Kazanci and Severcan, 2007), formation of reactive oxygen species (Nazarewicz et al, 2007), DNA damage by DNA-adducts or chromosomal aberrations, which have been found to occur in kidney and liver (Han and Liehr, 1992;Sargent et al, 1994). On the other hand, lower concentrations of tamoxifen (1 M and below) induced a gradual appearance of cell death starting to occur approximately 2-3 days after treatment .…”

Section: Autophagic Cell Deathmentioning

confidence: 99%

Cell death and autophagy: Cytokines, drugs, and nutritional factors

Bursch¹,

Karwan²,

Mayer³

et al. 2008

Toxicology

118

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Cells may use multiple pathways to commit suicide. In certain contexts, dying cells generate large amounts of autophagic vacuoles and clear large proportions of their cytoplasm, before they finally die, as exemplified by the treatment of human mammary carcinoma cells with the anti-estrogen tamoxifen (TAM, <= 1 mu M). Protein analysis during autophagic cell death revealed distinct proteins of the nuclear fraction including CST-pi and some proteasomal subunit constituents to be affected during autophagic cell death. Depending on the functional status of caspase-3, MCF-7 cells may switch between autophagic and apoptotic features of cell death [Fazi, B., Bursch, W., Fimia, G.M., Nardacci R., Piacentini, M., Di Sano, F., Piredda. L., 2008. Fenretinide induces autophagic cell death in caspase-defective breast cancer cells. Autophagy 4(4), 435-441]. Furthermore, the self-destruction of MCF-7 cells was found to be completed by phagocytosis of cell residues [Petrovski, G., Zahuczky, G., Katona, K., Vereb, G., Martinet. W., Nemes, Z., Bursch, W., Fesus, L., 2007. Clearance of dying autophagic cells of different origin by professional and non-professional phagocytes. Cell Death Diff. 14 (6),1117-1128]. Autophagy also constitutes a cell's strategy of defense upon cell damage by eliminating damaged bulk proteins/organelles. This biological condition may be exemplified by the treatment of MCF-7 cells with a necrogenic TAM-dose (10 mu M), resulting in the lysis of almost all cells within 24 h. However, a transient (1 h) challenge of MCF-7 cells with the same dose allowed the recovery of cells involving autophagy. Enrichment of chaperones in the insoluble cytoplasmic protein fraction indicated the formation of aggresomes, a potential trigger for autophagy. In a further experimental model HL60 cells were treated with TAM, causing dose-dependent distinct responses: 1-5 mu M TAM, autophagy predominant; 7-9 mu M, apoptosis predominant; 15 mu M, necrosis. These phenomena might be attributed to the degree of cell damage caused by tamoxifen, either by generating ROS, increasing membrane fluidity or forming DNA-adducts. Finally, autophagy constitutes a cell's major adaptive (survival) strategy in response to metabolic challenges such as glucose or amino acid deprivation, or starvation in general. Notably, the role of autophagy appears not to be restricted to nutrient recycling in order to maintain energy supply of cells and to adapt cell(organ) size to given physiological needs. For instance, using a newly established hepatoma cell line HCC-1.2, amino acid and glucose deprivation revealed a pro-apoptotic activity, additive to TGF-beta 1.The proapoptotic action of glucose deprivation was antagonized by 2-deoxyglucose, possibly by stabilizing the mitochondrial membrane involving the action of hexokinase II. These observations suggest that signaling cascades steering autophagy appear to provide links to those regulating cell number. Taken together, our data exemplify that a given cell may flexibly respond to type and degree of (micro)envir...

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“…Biological membranes are composed of extremely complex structures; thus, model membranes provide a highly convenient, simple method for studying drugmembrane interactions (Bangham, 1972;Engberts and Hoekstra, 1995;Kazanci and Severcan, 2007;Severcan et al, 2005). Despite its importance, studies on the interaction of celecoxib with membranes at a molecular level are very limited.…”

mentioning

confidence: 99%

Concentration-dependent differing actions of the nonsteroidal anti-inflammatory drug, celecoxib, in distearoyl phosphatidylcholine multilamellar vesicles

Sade¹,

Banerjee²,

Severcan³

2009

Journal of Liposome Research

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The interactions of the nonsteroidal anti-inflammatory drug, celecoxib, with 1,2-distearoyl-sn-glycero-3-phosphocholine multilamellar vesicles were studied as a function of temperature and different drug concentrations, using Fourier transform infrared spectroscopy, differential scanning calorimetry, and turbidity technique at 440 nm. Our studies reveal that celecoxib lowers the main phase-transition temperature and decreases the fluidity of the membranes at all concentrations. Celecoxib induced opposing effects on molecular order at different concentrations by increasing the ordering of the system at low concentrations and disordering it at high concentrations. Further, the drug increases the number of hydrogen bonds around the carbonyl groups at low concentrations in both phases, whereas the degree of dehydration increases at high concentrations in the gel phase. An evidence of phase separation has also been clearly observed at high concentrations. Thus, depending on the concentration used, celecoxib induces significant changes in the biophysical properties of membranes that may aid in understanding its mechanism of action.

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Concentration Dependent Different Action of Tamoxifen on Membrane Fluidity

Cited by 31 publications

References 35 publications

Biophysics in cancer: The relevance of drug-membrane interaction studies

Biophysics in cancer: The relevance of drug-membrane interaction studies

Cell death and autophagy: Cytokines, drugs, and nutritional factors

Concentration-dependent differing actions of the nonsteroidal anti-inflammatory drug, celecoxib, in distearoyl phosphatidylcholine multilamellar vesicles

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