The ER? membrane pool modulates the proliferation of pituitary tumours

Article

Authorship

SOSA, LILIANA DEL VALLE ; PETITI, JUAN PABLO ; Picech, Florencia ; Chumpen Ramirez, Sabrina Vanesa ; NICOLA, JUAN PABLO ; PÉREZ, PABLO ANÍBAL ; DE PAUL, ANA LUCIA ; Valdez Taubas, Javier ; Guitierrez, Silvina ; Torres, Alicia Ines

Date

2019

Publishing House and Editing Place

BioScientifica

Magazine

JOURNAL OF ENDOCRINOLOGY, vol. 240 (pp. 229-241) BioScientifica

Summary Information provided by the agent in SIGEVA

The molecular mechanisms underlying the ER? nuclear/cytoplasmic pool that modulates pituitary cell proliferation have been widely described, but it is still not clear how ER? is targeted to the plasma membrane. The aim of this study was to analyse ER? palmitoylation and the plasma membrane ER? (mER?) pool, and their participation in E2-triggered membrane-initiated signalling in normal and pituitary tumour cell growth. Cell cultures were prepared from anterior pituitaries of female Wistar rats a... The molecular mechanisms underlying the ER? nuclear/cytoplasmic pool that modulates pituitary cell proliferation have been widely described, but it is still not clear how ER? is targeted to the plasma membrane. The aim of this study was to analyse ER? palmitoylation and the plasma membrane ER? (mER?) pool, and their participation in E2-triggered membrane-initiated signalling in normal and pituitary tumour cell growth. Cell cultures were prepared from anterior pituitaries of female Wistar rats and tumour GH3 cells, and treated with 10 nM of oestradiol (E2). The basal expression of ER? was higher in tumour GH3 than in normal pituitary cells. Full-length palmitoylated ER? was observed in normal and pituitary tumour cells, demonstrating that E2 stimulation increased both, ER? in plasma membrane and ER? and caveolin-1 interaction after short-term treatment. In addition, the Dhhc7 and Dhhc21 palmitoylases were negatively regulated after sustained stimulation of E2 for 3 h. Although the uptake of BrdU into the nucleus in normal pituitary cells was not modified by E2, a significant increase in the GH3 tumoural cell, as well as ERK1/2 activation, with this effect being mimicked by PPT, a selective antagonist of ER?. These proliferative effects were blocked by ICI 182780 and the global inhibitor of palmitoylation. These findings indicate that ER? palmitoylation modulated the mER? pool and consequently the ERK1/2 pathway, thereby contributing to pituitary tumour cell proliferation. These results suggest that the plasma membrane ER? pool might be related to the proliferative behaviour of prolactinoma and may be a marker of pituitary tumour growth.