PMID- 16253280
OWN - NLM
STAT- MEDLINE
DCOM- 20060414
LR  - 20181201
IS  - 0024-3205 (Print)
IS  - 0024-3205 (Linking)
VI  - 78
IP  - 13
DP  - 2006 Feb 23
TI  - Different effects of estradiol and various antiestrogens on TNF-alpha-induced 
      changes of biochemical markers for growth and invasion of human breast cancer 
      cells.
PG  - 1464-8
AB  - In the field of estrogen therapy breast cancer risk is one of the most 
      controversially discussed topic. Actually, the as yet largest placebo-controlled 
      study, the Women's Health Initiative, rather showed a risk reduction, in contrast 
      to observational studies. In the present study we have investigated the effect of 
      estradiol on TNF-alpha-induced changes of various markers in human breast cancer 
      cells and compare it with the effect of the antiestrogens tamoxifen and 
      2-methoxyestradiol. MCF-7 cells were used for the experiments, the incubation 
      time was 96 h. TNF-alpha elicited a 3-4-fold increase of monocyte-attracting 
      protein-1 (MCP-1) and interleukin-8 (IL-8) as compared to the control value, 
      matrix metalloproteinase-9 (MMP-9) and vascular endothelial growth factor (VEGF) 
      were enhanced by 30 to 40%. E2 alone had no effect on MCP-1, slightly reduced the 
      synthesis of MMP-9 and increased VEGF concentrations by about 20%. In combination 
      with TNF, E2 induced a further stimulation of MCP-1, IL-8 and VEGF, whereby the 
      MMP-9 synthesis was not changed. Tamoxifen and the endogenous estradiol 
      metabolite 2-methoxyestradiol seem to be able to partly inhibit the action of 
      TNF-alpha and estradiol. Our results suggest that estrogens may slightly increase 
      tumor growth and spreading beyond the effect of chemokines such as TNF-alpha. 
      However, the magnitude of this E2 effect seems to be marginal as compared to the 
      effect of TNF-alpha alone. The risk of recurrence of breast cancer in patients 
      taking hormone therapy after breast cancer may be slightly enhanced by estrogens, 
      but seems mainly to be driven by the potency of still existing tumor cells to 
      secrete chemokines which can stimulate tumor growth and spreading.
FAU - Seeger, H
AU  - Seeger H
AD  - Section of Endocrinology and Menopause, University Women's Hospital, 
      Calwerstrasse 7 72 076 Tuebingen Germany.
FAU - Wallwiener, D
AU  - Wallwiener D
FAU - Mueck, A O
AU  - Mueck AO
LA  - eng
PT  - Journal Article
DEP - 20051025
PL  - Netherlands
TA  - Life Sci
JT  - Life sciences
JID - 0375521
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (Estrogen Receptor Modulators)
RN  - 0 (Interleukin-8)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 094ZI81Y45 (Tamoxifen)
RN  - 17197F0KYM (afimoxifene)
RN  - 4TI98Z838E (Estradiol)
RN  - 6I2QW73SR5 (2-Methoxyestradiol)
SB  - IM
MH  - 2-Methoxyestradiol
MH  - Apoptosis/drug effects
MH  - Biomarkers, Tumor/*metabolism
MH  - Breast Neoplasms
MH  - Cell Division/drug effects
MH  - Cell Line, Tumor
MH  - Estradiol/analogs & derivatives/*pharmacology
MH  - Estrogen Receptor Modulators/*pharmacology
MH  - Female
MH  - Humans
MH  - Interleukin-8/metabolism
MH  - Neoplasm Invasiveness
MH  - Tamoxifen/analogs & derivatives/pharmacology
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 2005/10/29 09:00
MHDA- 2006/04/15 09:00
CRDT- 2005/10/29 09:00
PHST- 2005/04/25 00:00 [received]
PHST- 2005/07/12 00:00 [accepted]
PHST- 2005/10/29 09:00 [pubmed]
PHST- 2006/04/15 09:00 [medline]
PHST- 2005/10/29 09:00 [entrez]
AID - S0024-3205(05)00993-8 [pii]
AID - 10.1016/j.lfs.2005.07.042 [doi]
PST - ppublish
SO  - Life Sci. 2006 Feb 23;78(13):1464-8. doi: 10.1016/j.lfs.2005.07.042. Epub 2005 
      Oct 25.