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Differing Mechanisms of Death Induction by Fluorinated Taxane SB-T-12854 in Breast Cancer Cells.

Abstract Classical taxanes are routinely used in cancer therapy. In this study, mechanisms involved in death induction by the novel fluorine-containing taxane SB-T-12854 were investigated.
PMID
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Authors

Mayor MeshTerms
Keywords

Bcl-2 proteins

SB-T-12854

breast cancer cells

caspases

cytochrome c release

Journal Title anticancer research
Publication Year Start




PMID- 28373418
OWN - NLM
STAT- MEDLINE
DA  - 20170404
DCOM- 20170413
LR  - 20170413
IS  - 1791-7530 (Electronic)
IS  - 0250-7005 (Linking)
VI  - 37
IP  - 4
DP  - 2017 Apr
TI  - Differing Mechanisms of Death Induction by Fluorinated Taxane SB-T-12854 in
      Breast Cancer Cells.
PG  - 1581-1590
AB  - BACKGROUND/AIM: Classical taxanes are routinely used in cancer therapy. In this
      study, mechanisms involved in death induction by the novel fluorine-containing
      taxane SB-T-12854 were investigated. MATERIALS AND METHODS: We employed breast
      cancer SK-BR-3, MCF-7 and T47D cell lines to assess activation of individual
      caspases, changes in the expression of proteins of the Bcl-2 family, and the
      release of pro-apoptotic factors from mitochondria into the cytosol after
      SB-T-12854 treatment. RESULTS: Caspase-2, -8, and -9 were activated in SK-BR-3
      and MCF-7 cells. Only caspase-8 was activated in T47D cells. Caspase-7 and -6
      were activated in all tested cells while caspase-3 was activated only in SK-BR-3 
      cells. Pro-apoptotic Bad protein seems to be important for cell death induction
      in all tested cells. Anti-apoptotic Bcl-2 and pro-apoptotic Bim, Bok, Bid and Bik
      seem to be also associated with cell death induction in some of the tested cells.
      The mitochondrial apoptotic pathway was significantly activated in association
      with the release of cytochrome c and Smac from mitochondria, but only in SK-BR-3 
      cells, not in MCF-7 and T47D cells. CONCLUSION: Cell death induced by SB-T-12854,
      in the tested breast cancer cells, differs regarding activation of caspases,
      changes in levels of pro-apoptotic and anti-apoptotic proteins of the Bcl-2
      family and activation of the mitochondrial apoptotic pathway.
CI  - Copyright(c) 2017, International Institute of Anticancer Research (Dr. George J. 
      Delinasios), All rights reserved.
FAU - Jelinek, Michael
AU  - Jelinek M
AD  - Department of Cell and Molecular Biology, Third Faculty of Medicine, Charles
      University, Prague, Czech Republic.
FAU - Kabelova, Adela
AU  - Kabelova A
AD  - Department of Cell and Molecular Biology, Third Faculty of Medicine, Charles
      University, Prague, Czech Republic.
FAU - Sramek, Jan
AU  - Sramek J
AD  - Department of Cell and Molecular Biology, Third Faculty of Medicine, Charles
      University, Prague, Czech Republic.
FAU - Seitz, Joshua
AU  - Seitz J
AD  - Institute of Chemical Biology and Drug Discovery, State University of New York at
      Stony Brook, Stony Brook, NY, U.S.A.
FAU - Ojima, Iwao
AU  - Ojima I
AD  - Institute of Chemical Biology and Drug Discovery, State University of New York at
      Stony Brook, Stony Brook, NY, U.S.A.
FAU - Kovar, Jan
AU  - Kovar J
AD  - Department of Cell and Molecular Biology, Third Faculty of Medicine, Charles
      University, Prague, Czech Republic [email protected]
LA  - eng
PT  - Journal Article
PL  - Greece
TA  - Anticancer Res
JT  - Anticancer research
JID - 8102988
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (Hydrocarbons, Fluorinated)
RN  - 0 (Taxoids)
RN  - EC 3.4.22.- (Caspases)
SB  - IM
MH  - Apoptosis/*drug effects
MH  - Biomarkers, Tumor/metabolism
MH  - Blotting, Western
MH  - Breast Neoplasms/drug therapy/*pathology
MH  - Caspases/metabolism
MH  - Cell Proliferation/*drug effects
MH  - Female
MH  - Humans
MH  - Hydrocarbons, Fluorinated/*pharmacology
MH  - Taxoids/*pharmacology
MH  - Tumor Cells, Cultured
OTO - NOTNLM
OT  - *Bcl-2 proteins
OT  - *SB-T-12854
OT  - *breast cancer cells
OT  - *caspases
OT  - *cytochrome c release
EDAT- 2017/04/05 06:00
MHDA- 2017/04/14 06:00
CRDT- 2017/04/05 06:00
PHST- 2017/01/31 [received]
PHST- 2017/03/15 [revised]
PHST- 2017/03/20 [accepted]
AID - 37/4/1581 [pii]
AID - 10.21873/anticanres.11488 [doi]
PST - ppublish
SO  - Anticancer Res. 2017 Apr;37(4):1581-1590.

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