Progesterone signaling in breast and endometrium

Ballaré, Cecilia; Vallejo, Griselda; Vicent, Guillermo P.; Saragüeta, Patricia; Beato, Miguel

doi:10.1016/j.jsbmb.2006.09.030

Cited by 37 publications

(20 citation statements)

References 31 publications

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“…In this study, we showed that phosphorylation of AKT was inhibited in CL treated with DAPT and that this effect was reversed with coincubation with progesterone. In this regard, it has been described that, in addition to transcriptional effects, progesterone activates the SRC/ ERK1/2 and PI3K/AKT pathways in breast cancer and endometrial stroma cells (Ballare et al 2006, Lee & Kim 2014. Our results suggest a similar mechanism in luteal cells, strengthening the hypothesis that an association exists between the antiapoptotic action of progesterone and Notch/PI3K/AKT signaling.…”

Section: Link Between Notch and Progesterone In CL Functionsupporting

confidence: 86%

A link between Notch and progesterone maintains the functionality of the rat corpus luteum

et al. 2015

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In this study, we investigated the interaction between the Notch pathway and progesterone to maintain the functionality of the corpus luteum (CL). When Notch signaling is activated, the g-secretase complex releases the active intracellular domains (NICD) of their receptors, which exert survival effects. We designed studies to analyze whether the in vitro inhibition of Notch affects progesterone production, steroidogenic regulators, apoptotic parameters, and signaling transduction pathways in the cultures of CL isolated from pregnant and superovulated rats. We detected a decrease in progesterone production when corpora lutea (CL) were incubated with N-(N-(3,5-difluorophenacetyl-L-alanyl))-S-phenylglycine t-butyl ester (DAPT), a g-secretase inhibitor. This effect could be in part due to the decrease detected in the CL protein levels of P450scc because STAR and 3b-hydroxysteroid dehydrogenase were not affected by Notch inhibition. Besides, the addition of aminoglutethimide to the CL culture medium decreased NICD of NOTCH1. We observed an increase in the expression of active CASPASE3 (CASP3) after inhibition by Notch, which was reversed by the presence of progesterone. The BAX:BCLX L ratio was increased in CL treated with DAPT and the presence of progesterone reversed this effect. In addition, phosphorylation of AKT was inhibited in CL treated with DAPT, but had no effect on ERK activation. To demonstrate that the action of DAPT is specifically related with the inhibition of Notch, CLs were incubated with DLL4 antibody and a decrease in progesterone production was detected. These results suggest the existence of a novel link between progesterone and the Notch signaling pathway to maintain the functionality of the CL.

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Section: Link Between Notch and Progesterone In CL Functionsupporting

confidence: 86%

A link between Notch and progesterone maintains the functionality of the rat corpus luteum

et al. 2015

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“…In human breast cancer cells, P4 induces rapid and transient activation of PI3K-Akt pathway in a P4R-dependent manner (Migliaccio et al, 1998;Castoria et al, 2001). It was reported that progestins rapidly activated PI3K-Akt pathway via P4R Ballare et al, 2006). However, our results here showed that the PI3K-mediated neuroprotection by P4 administered at 72 h post-MCAO is P4R-independent.…”

Section: P4r-dependent Erk Activation At 24-48 H After Strokecontrasting

confidence: 72%

Time-Window of Progesterone Neuroprotection After Stroke and Its Underlying Molecular Mechanisms

Cai¹,

Sokabe²,

Chen³

2012

Advances in the Preclinical Study of Ischemic Stroke

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“…Other signaling pathways have been reported to be rapidly activated by progestin and mediate their effects, including cell proliferation of breast cancer cells (6,22). Hormonal activation of the MMTV promoter depends not only on PR interaction with several HREs but also on the hormone-activated ER␣/c-Src/Ras/Erk pathway (62).…”

Section: Discussionmentioning

confidence: 99%

Progesterone Induction of the 11β-Hydroxysteroid Dehydrogenase Type 2 Promoter in Breast Cancer Cells Involves Coordinated Recruitment of STAT5A and Progesterone Receptor to a Distal Enhancer and Polymerase Tracking

Subtil‐Rodríguez

Millán-Ariño

Quiles

et al. 2008

Molecular and Cellular Biology

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Steroid hormone receptors (SHRs) are considered nuclear transcription factors that, upon activation by binding with their corresponding ligands, regulate the expression of different target genes. Ligand-activated SHRs act either by binding as dimers to their hormone-responsive elements (HREs) at promoters or by interaction with other DNA-bound factors. In both cases, the process results in the recruitment of coregulators, chromatin remodeling complexes, and the general transcriptional machinery (7). However, SHRs also modulate gene expression by activation of cytoplasmic signaling pathways (nongenomic actions) (22).The estrogen receptor (ER) binds to c-Src and to the phosphoinositol 3-kinase (PI3K) regulatory subunit, activating the Src/Ras/Erk and PI3K/Akt pathways, respectively (15, 41). These rapid effects triggered by hormones have been associated with their proliferative role. Ligand-activated progesterone receptor (PR) activates the Src/Ras/Erk pathway indirectly via an interaction with ER in the absence of estrogens (5), although direct interaction and activation of c-Src by PR has also been reported (11).The relationship between SHRs' direct transcriptional effects and those mediated by activation of cytoplasmic kinase cascades in the hormone-inducible mouse mammary tumor virus (MMTV) promoter was recently investigated (62). After progesterone treatment, Erk and Msk1 are activated and recruited with phosphorylated PR to the promoter, where histone H3 is phosphorylated and acetylated locally. These H3 modifications seem to be a key switch for the exchange of a repressive complex containing HP1␥ by coactivators, chromatin remodeling complexes, and RNA polymerase II (RNAP II). Thus, rapid kinase activation by progestin may participate in induction of PR direct target genes by preparing the chromatin for transcription, indicating that both PR actions cross talk to each other.In breast cancer cells, progestin also induces activation of the JAK/STAT (signal transducer and activator of transcription) pathway and the subsequent phosphorylation of STAT proteins (47). The activation of the JAK/STAT pathway is initiated by cytokines or growth factors binding to their specific membrane-associated receptor. Receptor dimerization leads to JAK activation, which sequentially autophosphorylates and phosphorylates the receptor and STAT proteins. STAT proteins dimerize, translocate to the nucleus, and bind to DNA

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Progesterone signaling in breast and endometrium

Cited by 37 publications

References 31 publications

A link between Notch and progesterone maintains the functionality of the rat corpus luteum

A link between Notch and progesterone maintains the functionality of the rat corpus luteum

Time-Window of Progesterone Neuroprotection After Stroke and Its Underlying Molecular Mechanisms

Progesterone Induction of the 11β-Hydroxysteroid Dehydrogenase Type 2 Promoter in Breast Cancer Cells Involves Coordinated Recruitment of STAT5A and Progesterone Receptor to a Distal Enhancer and Polymerase Tracking

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