Prolactin - Tren/Deca

[Swifto]

J Steroid Biochem Mol Biol. 2002 Oct;82(2-3):263-8.

Estradiol stimulates expression of two human prolactin receptor isoforms with alternative exons-1 in T47D breast cancer cells.

Leondires MP, Hu ZZ, Dong J, Tsai-Morris CH, Dufau ML.
Source

National Institute of Child Health and Human Development, Section Molecular Endocrinology, Endocrinology and Reproduction Research Branch, National Institutes of Health, Bethesda, MD 20892-4510, USA.
Abstract

Human prolactin receptor (hPRLR) expression is regulated by estradiol-17beta (E(2)) in vivo in animal tissues, and in vitro in normal human endometrial cells and in MCF7 human breast cancer cells. The objective of this study was to determine the effect of E(2) on the expression of two recently described hPRLR isoforms with distinct exons-1, hE1(3) and hE1(N1) that are transcribed from the generic hPIII promoter, also present in the rat and mouse, and the human-specific promoter hP(N1), respectively. Also, to determine the effect of estradiol on the hPIII promoter activity in cancer cells. T47D breast cancer cells were examined using quantitative competitive RT-PCR for the level of expression of two alternative non-coding exon-1 transcripts, hE1(3) and hE1(N1) following incubation with E(2) in presence or absence of the E(2) receptor antagonist ICI 182,***. The effects of estradiol were also evaluated in cells transiently transfected with constructs of hPIII promoter luciferase reporter gene. E(2) significantly increased the expression of both hPRLR mRNA transcripts, hE1(3) and hE1(N1). In transfection studies E(2) activated the hPIII promoter. This effect of estradiol was markedly inhibited by coincubation with the E(2) receptor antagonist. Our results demonstrate a stimulatory effect of estradiol on the expression of hPRLR mRNA species with alternative exons-1, hE1(3) and hE1(N1) possibly through activation of their corresponding promoters. The lack of a formal ERE in these promoters suggested that the effect of estradiol is mediated through association of the activated ER with relevant DNA binding transfactor(s). These findings support the role of E(2) in the regulation of hPRLR expression in human breast cancer cell lines.

PMID:
12477494
[PubMed - indexed for MEDLINE]

Not ideal as we also know that normal brest tissue can sometimes respnd differently than cancer cell tissue (PgR expression).

[Atomini]

Although there isnt solid data on prolactin LEVELS raising from 19-Nors, I'm pretty sure the estrogen receptor is a co-binding factor in prolactin receptor expression (PRLR). This can make us far more sensitive to PRL even if its not increased or wildly out of range. This theory also fits well with the ER being the causitive factor in PRL issues.

Yes, agreed, which is also why for the most part, controlling E2 levels should control Prolactin.

Wow guys please continue. I am learning and thinking all at the same time

And I'm close to running test and 2 nor 19's together and this is very helpful for me

Getting any bloodwork done while on that? Would be interesting to see what the readings are for a cycle with two 19-nors.

[Capebuffalo]

Yes, agreed, which is also why for the most part, controlling E2 levels should control Prolactin.



Getting any bloodwork done while on that? Would be interesting to see what the readings are for a cycle with two 19-nors.

My thought ( and I have spoken to others ) is if I run 800 mgs of tren a
Is there a difference in running 400 mgs NPP and 400 mgs tren a
It is still 800 mgs of a nor 19. Not trying to hijack but interested if extra
precautions need to be taken fro prolactin
I'm on 8 reload 2 deload so blood work not accurate for a start point.

[jimmyinkedup]

J Steroid Biochem Mol Biol. 2002 Oct;82(2-3):263-8.

Estradiol stimulates expression of two human prolactin receptor isoforms with alternative exons-1 in T47D breast cancer cells.

Leondires MP, Hu ZZ, Dong J, Tsai-Morris CH, Dufau ML.
Source

National Institute of Child Health and Human Development, Section Molecular Endocrinology, Endocrinology and Reproduction Research Branch, National Institutes of Health, Bethesda, MD 20892-4510, USA.
Abstract

Human prolactin receptor (hPRLR) expression is regulated by estradiol-17beta (E(2)) in vivo in animal tissues, and in vitro in normal human endometrial cells and in MCF7 human breast cancer cells. The objective of this study was to determine the effect of E(2) on the expression of two recently described hPRLR isoforms with distinct exons-1, hE1(3) and hE1(N1) that are transcribed from the generic hPIII promoter, also present in the rat and mouse, and the human-specific promoter hP(N1), respectively. Also, to determine the effect of estradiol on the hPIII promoter activity in cancer cells. T47D breast cancer cells were examined using quantitative competitive RT-PCR for the level of expression of two alternative non-coding exon-1 transcripts, hE1(3) and hE1(N1) following incubation with E(2) in presence or absence of the E(2) receptor antagonist ICI 182,***. The effects of estradiol were also evaluated in cells transiently transfected with constructs of hPIII promoter luciferase reporter gene. E(2) significantly increased the expression of both hPRLR mRNA transcripts, hE1(3) and hE1(N1). In transfection studies E(2) activated the hPIII promoter. This effect of estradiol was markedly inhibited by coincubation with the E(2) receptor antagonist. Our results demonstrate a stimulatory effect of estradiol on the expression of hPRLR mRNA species with alternative exons-1, hE1(3) and hE1(N1) possibly through activation of their corresponding promoters. The lack of a formal ERE in these promoters suggested that the effect of estradiol is mediated through association of the activated ER with relevant DNA binding transfactor(s). These findings support the role of E(2) in the regulation of hPRLR expression in human breast cancer cell lines.

PMID:
12477494
[PubMed - indexed for MEDLINE]

Not ideal as we also know that normal brest tissue can sometimes respnd differently than cancer cell tissue (PgR expression).

Its tricky because i definitively recall reading that e2 did not effect PRLR expression in the pituitary at all. I will look to see if i can find it. Ive also read that testosterone has an inhibitory effect and estrogen a stimulatory one. This one is all over.
I will say this ...show me one set of bloodwork where e2 is manged properly where a progestin increased prolactin. I dont think you can do it (not you Swifto - commenting on the general thread topic)..because i dont think it does.