PMID- 8547183
OWN - NLM
STAT- MEDLINE
DCOM- 19960220
LR  - 20190830
IS  - 0960-0760 (Print)
IS  - 0960-0760 (Linking)
VI  - 55
IP  - 5-6
DP  - 1995 Dec
TI  - The role and proposed mechanism by which oestradiol 17 beta-hydroxysteroid 
      dehydrogenase regulates breast tumour oestrogen concentrations.
PG  - 565-72
AB  - Synthesis of the biologically active oestrogen, oestradiol, within breast tumours 
      makes an important contribution to the high concentrations of oestrogens which 
      are present in malignant breast tissues. In breast tumours, oestrone is 
      preferentially converted to oestradiol by the Type I oestradiol 17 
      beta-hydroxysteroid dehydrogenase (E2DH). Several growth factors, such as 
      insulin-like growth factor Type I, and cytokines, such as Tumour Necrosis Factor 
      alpha (TNF alpha), have been shown to stimulate E2DH activity in MCF-7 breast 
      cancer cells. As little is known about the regulation of Type I E2DH expression 
      and activity in other breast cancer cell lines, the expression and activity of 
      this enzyme was examined in other oestrogen receptor positive and also oestrogen 
      receptor negative breast cancer cell lines. As it is possible that E2DH activity 
      may be limited by co-factor availability, the effects of exogenous co-factors on 
      enzyme activity in these cell lines was also investigated. For T47D and BT20 
      breast cancer cells, the addition of exogenous co-factors was found to enhance 
      enzyme activity. TNF alpha, in addition to stimulating E2DH activity in MCF-7 
      cells, also increased activity in T47D and MDA-MB-231 cells, although to a lesser 
      extent than in MCF-7 cells. An investigation of signalling pathways involved in 
      the regulation of E2DH activity revealed that stimulation of both the protein 
      kinase C (PKC) and PKA pathways may be involved in regulation of E2DH activity. 
      As several growth factors and cytokines have now been found to be involved in 
      regulating E2DH activity, the role that macrophages and lymphocytes have in 
      supplying these factors and the mechanism by which these factors may stimulate 
      tumour growth, is also reviewed.
FAU - Duncan, L J
AU  - Duncan LJ
AD  - Unit of Metabolic Medicine, St Mary's Hospital Medical School, Imperial College 
      of Science, Technology and Medicine, London, U.K.
FAU - Reed, M J
AU  - Reed MJ
LA  - eng
PT  - Journal Article
PL  - England
TA  - J Steroid Biochem Mol Biol
JT  - The Journal of steroid biochemistry and molecular biology
JID - 9015483
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Estrogens)
RN  - 0 (Naphthalenes)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Estrogen)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (calphostin complex)
RN  - 1F7A44V6OU (Colforsin)
RN  - 53-59-8 (NADP)
RN  - 5688UTC01R (Tretinoin)
RN  - EC 1.1.1.62 (Estradiol Dehydrogenases)
RN  - EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases)
RN  - EC 2.7.11.13 (Protein Kinase C)
RN  - NI40JAQ945 (Tetradecanoylphorbol Acetate)
SB  - IM
MH  - Breast/*metabolism
MH  - Colforsin/pharmacology
MH  - Cyclic AMP-Dependent Protein Kinases/physiology
MH  - Enzyme Inhibitors/pharmacology
MH  - Estradiol Dehydrogenases/*metabolism
MH  - Estrogens/*metabolism
MH  - Female
MH  - Gene Expression Regulation, Enzymologic/drug effects
MH  - Humans
MH  - NADP/metabolism
MH  - Naphthalenes/pharmacology
MH  - Protein Kinase C/physiology
MH  - RNA, Messenger/genetics
MH  - Receptors, Estrogen/metabolism
MH  - Signal Transduction
MH  - Tetradecanoylphorbol Acetate/pharmacology
MH  - Tretinoin/pharmacology
MH  - Tumor Cells, Cultured
MH  - Tumor Necrosis Factor-alpha/pharmacology
EDAT- 1995/12/01 00:00
MHDA- 1995/12/01 00:01
CRDT- 1995/12/01 00:00
PHST- 1995/12/01 00:00 [pubmed]
PHST- 1995/12/01 00:01 [medline]
PHST- 1995/12/01 00:00 [entrez]
AID - 10.1016/0960-0760(95)00207-3 [doi]
PST - ppublish
SO  - J Steroid Biochem Mol Biol. 1995 Dec;55(5-6):565-72. doi: 
      10.1016/0960-0760(95)00207-3.