The mechanism of methylselenocysteine and docetaxel synergistic activity in prostate cancer cells.

The mechanism of methylselenocysteine and docetaxel synergistic activity in prostate cancer cells. Research Abstract Details 

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The mechanism of methylselenocysteine and docetaxel synergistic activity in prostate cancer cells. Abstract Text:

Rami G Azrak,Cheryl L Frank,Xiang Ling,Harry K Slocum,Fengzhi Li,Barbara A Foster,Youcef M Rustum,

The study was designed to evaluate the combination treatment of methylselenocysteine (MSeC) and docetaxel and to delineate the underlying mechanism associated with observed in vitro synergy between MSeC and docetaxel in prostate cancer cells. Cells were treated with different concentrations and schedules (concurrent or sequential) of MSeC and docetaxel alone or in combination. Cell growth/death was assessed with sulforhodamine B assay, trypan blue assay, and time-lapse video. Loewe synergism/antagonism model was used to determine whether the combination effect was additive, synergistic, or antagonistic. Apoptosis and caspase-3 activity were evaluated with cell death ELISA assay and caspase activity assay, respectively. Synergy between MSeC and docetaxel was further assessed in the presence and absence of z-VAD-fmk, a pan-caspase inhibitor. Effect of MSeC and docetaxel alone or in combination on the cellular expression of the antiapoptotic protein survivin was measured with Western blot analyses. Pretreatment with MSeC was crucial to enhance docetaxel antitumor activity. The enhanced antitumor activity of the sequential combination treatment of MSeC and docetaxel (MSeC/docetaxel) was highly synergistic. Apoptosis increased after MSeC/docetaxel, compared with each drug alone or concurrent treatment. Pretreatment with z-VAD-fmk converted the synergy into antagonism, suggesting that the synergy is caspase-dependent apoptosis. The survivin level was down-regulated following MSeC/docetaxel treatment when compared with each drug alone. In conclusion, pretreatment with MSeC was essential to markedly sensitize cells to docetaxel. The synergy between MSeC and docetaxel in C2G prostate cancer cells is associated with increased level of caspase-dependent apoptosis and decreased level of survivin.

The mechanism of methylselenocysteine and docetaxel synergistic activity in prostate cancer cells. Publishing Authors By Initials

RG Azrak,CL Frank,X Ling,HK Slocum,F Li,BA Foster,YM Rustum,

For similar organic chemicals: hydrocarbons: hydrocarbons, cyclic: hydrocarbons, alicyclic: cycloparaffins: cyclodecanes: taxoids research abstracts see: organic chemicals: hydrocarbons: hydrocarbons, cyclic: hydrocarbons, alicyclic: cycloparaffins: cyclodecanes: taxoids research

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MEDLINE DATE:

The mechanism of methylselenocysteine and docetaxel synergistic activity in prostate cancer cells. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Molecular cancer therapeutics

VOLUME: 5

Page Numbers: 2540-8

Journal Abbreviation: Mol. Cancer Ther.

ISSN: 1535-7163

DAY: 3

MONTH: Oct

YEAR: 2006

The mechanism of methylselenocysteine and docetaxel synergistic activity in prostate cancer cells. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 101132535

The mechanism of methylselenocysteine and docetaxel synergistic activity in prostate cancer cells. Keywords Mesh Terms:

KEYWORDS: Taxoids

MESH TERMS: pharmacology

Chemical & Substance for Abstract: The mechanism of methylselenocysteine and docetaxel synergistic activity in prostate cancer cells. Information

Substance Name: Caspase 3

Registry Number: EC 3.4.22.-

Grant and Affiliation Information for The mechanism of methylselenocysteine and docetaxel synergistic activity in prostate cancer cells.

AFFILIATION: Department of Cancer Biology, Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USA. azrak@roswellpark.org

Country: United States

AGENCY: United States NCI

GRANT: CA65761

ACRONYM: CA

MEDLINETA: Mol Cancer Ther

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