PMID- 22866165
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20121002
LR  - 20211021
IS  - 1837-9664 (Electronic)
IS  - 1837-9664 (Linking)
VI  - 3
DP  - 2012
TI  - Effect of tumour necrosis factor-alpha on estrogen metabolic pathways in breast 
      cancer cells.
PG  - 310-21
LID - 10.7150/jca.4584 [doi]
AB  - Tumor necrosis factor-alpha (TNF-alpha) is a proinflammatory cytokine that has been 
      linked to breast cancer development. Estrogen metabolic pathway is also involved 
      in breast carcinogenesis and DNA adducts formation. In this study we investigated 
      the effect of TNF-alpha on the estrogen metabolic pathway in MCF-7, a breast cancer 
      cell line. Capillary liquid chromatography/mass spectrometry (LC/MS) and High 
      performance liquid chromatography (HPLC) were used for analysis of estrogen 
      metabolites and estrogen-DNA adducts levels respectively. Reporter gene assay, 
      Real time reverse transcription polymerase chain reaction (real time RT-PCR) and 
      Western blot were used to assess the expression of estrogen metabolizing genes 
      and enzymes. TNF-alpha significantly increased the total EM and decreased the estrone 
      (E1) / 17-beta estradiol (E2) ratio. Moreover, it altered the expression of genes 
      and enzymes involved in E2 activation and deactivation pathways e.g. Cytochrome 
      P-450 1A1 (CYP1A1), Cytochrome P-450 1B1 (CYP1B1), Catechol-O-methyl transferase 
      (COMT) and Nicotinamide adenine dinucleotide phosphate-quinone oxidoreductase 1 
      (NQO1). In addition, there were increased levels of some catechol estrogens e.g. 
      4-hydroxy-estrone (4-OHE1) and 2-hydroxyestradiol (2-OHE2) with decreased levels 
      of methylated catechols e.g. 2-methoxy estradiol (2-MeOE2). DNA adducts 
      especially 4-OHE1-[2]-1-N3 Adenine was significantly increased. TNF-alpha directs the 
      estrogen metabolism into more hormonally active and carcinogenic products in 
      MCF-7. This may implicate a new possible explanation for inflammation associated 
      breast cancer.
FAU - Kamel, Marwa
AU  - Kamel M
AD  - 1. Unit of Pharmacology, Department of Cancer Biology, National Cancer Institute, 
      Cairo University, Egypt.
FAU - Shouman, Samia
AU  - Shouman S
FAU - El-Merzebany, Mahmoud
AU  - El-Merzebany M
FAU - Kilic, Gokhan
AU  - Kilic G
FAU - Veenstra, Timothy
AU  - Veenstra T
FAU - Saeed, Muhammad
AU  - Saeed M
FAU - Wagih, Mohamed
AU  - Wagih M
FAU - Diaz-Arrastia, Concepcion
AU  - Diaz-Arrastia C
FAU - Patel, Deepa
AU  - Patel D
FAU - Salama, Salama
AU  - Salama S
LA  - eng
PT  - Journal Article
DEP - 20120706
PL  - Australia
TA  - J Cancer
JT  - Journal of Cancer
JID - 101535920
PMC - PMC3408695
OTO - NOTNLM
OT  - Breast cancer
OT  - DNA adducts.
OT  - Estrogen metabolites
OT  - Estrogen metabolizing genes and enzymes
OT  - Tumor necrosis factor-alpha
COIS- Competing Interests: The authors have declared that no competing interest exists.
EDAT- 2012/08/07 06:00
MHDA- 2012/08/07 06:01
PMCR- 2012/01/01
CRDT- 2012/08/07 06:00
PHST- 2012/05/12 00:00 [received]
PHST- 2012/06/19 00:00 [accepted]
PHST- 2012/08/07 06:00 [entrez]
PHST- 2012/08/07 06:00 [pubmed]
PHST- 2012/08/07 06:01 [medline]
PHST- 2012/01/01 00:00 [pmc-release]
AID - jcav03p0310 [pii]
AID - 10.7150/jca.4584 [doi]
PST - ppublish
SO  - J Cancer. 2012;3:310-21. doi: 10.7150/jca.4584. Epub 2012 Jul 6.