scholarly journals Minireview: C2- and C4-position 17β-estradiol metabolites and their relation to breast cancer

BIOCELL ◽  
2009 ◽  
Vol 33 (3) ◽  
pp. 137-140 ◽  
Author(s):  
ANNIE JOUBERT ◽  
HERMIA VAN ZYL ◽  
JOHANNES LAURENS ◽  
MONA-LIZA LOTTERING
Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 623
Author(s):  
Marit Rasmussen ◽  
Susanna Tan ◽  
Venkata S. Somisetty ◽  
David Hutin ◽  
Ninni Elise Olafsen ◽  
...  

ADP-ribosylation is a post-translational protein modification catalyzed by a family of proteins known as poly-ADP-ribose polymerases. PARP7 (TIPARP; ARTD14) is a mono-ADP-ribosyltransferase involved in several cellular processes, including responses to hypoxia, innate immunity and regulation of nuclear receptors. Since previous studies suggested that PARP7 was regulated by 17β-estradiol, we investigated whether PARP7 regulates estrogen receptor α signaling. We confirmed the 17β-estradiol-dependent increases of PARP7 mRNA and protein levels in MCF-7 cells, and observed recruitment of estrogen receptor α to the promoter of PARP7. Overexpression of PARP7 decreased ligand-dependent estrogen receptor α signaling, while treatment of PARP7 knockout MCF-7 cells with 17β-estradiol resulted in increased expression of and recruitment to estrogen receptor α target genes, in addition to increased proliferation. Co-immunoprecipitation assays revealed that PARP7 mono-ADP-ribosylated estrogen receptor α, and mass spectrometry mapped the modified peptides to the receptor’s ligand-independent transactivation domain. Co-immunoprecipitation with truncated estrogen receptor α variants identified that the hinge region of the receptor is required for PARP7-dependent mono-ADP-ribosylation. These results imply that PARP7-mediated mono-ADP-ribosylation may play an important role in estrogen receptor positive breast cancer.


2019 ◽  
Vol 73 ◽  
pp. 909-919
Author(s):  
Ewa Sawicka ◽  
Arkadiusz Woźniak ◽  
Małgorzata Drąg-Zalesińska ◽  
Agnieszka Piwowar

Oncological diseases, due to the still increasing morbidity and mortality, are one of the main problems of modern medicine. Cancer of the mammary gland is the most common cancer among women around the world, and is the second cause of cancer deaths in this group, immediately after lung cancer. This kind of cancer belongs to an estrogen-dependent cancer, with proven associations with hormonal disorders in the body, occurring especially in the perimenopausal period and among women using hormone replacement therapy, as well as a result of the action of various xenobiotics that may interact with the estrogen receptor. Hormone steroids are widely used in medicine and their side effects are constantly discussed. The role of these compounds and their metabolites in maintaining hormonal balance is well understood, while many studies indicate the possible contribution of these steroids in the progression of the cancer process, especially in mammary gland tissue. Therefore, the genotoxic action of this group of compounds is still studied. Due to the limited number of scientific reports, the aim of this paper was to review and critically analyze data from the literature regarding the participation of estrogens (17β-estradiol) and their metabolites (2-methoxy estradiol, 4-hydroxy estradiol, 16α-hydroxyestrone) in the induction of carcinogenesis in mammary gland, in particular concerning the genotoxic activity of 17β-estradiol metabolites.


2006 ◽  
Vol 99 (1) ◽  
pp. 209-220 ◽  
Author(s):  
Wan Ru Lee ◽  
Chien-Cheng Chen ◽  
Shengxi Liu ◽  
Stephen Safe

Sign in / Sign up

Export Citation Format

Share Document