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Estrogen promotes the survival and pulmonary metastasis of tuberin-null cells.

Abstract：

:Lymphangioleiomyomatosis (LAM) is an often fatal disease primarily affecting young women in which tuberin (TSC2)-null cells metastasize to the lungs. The mechanisms underlying the striking female predominance of LAM are unknown. We report here that 17-beta-estradiol (E(2)) causes a 3- to 5-fold increase in pulmonary metastases in male and female mice, respectively, and a striking increase in circulating tumor cells in mice bearing tuberin-null xenograft tumors. E(2)-induced metastasis is associated with activation of p42/44 MAPK and is completely inhibited by treatment with the MEK1/2 inhibitor, CI-1040. In vitro, E(2) inhibits anoikis of tuberin-null cells. Finally, using a bioluminescence approach, we found that E(2) enhances the survival and lung colonization of intravenously injected tuberin-null cells by 3-fold, which is blocked by treatment with CI-1040. Taken together these results reveal a new model for LAM pathogenesis in which activation of MEK-dependent pathways by E(2) leads to pulmonary metastasis via enhanced survival of detached tuberin-null cells.

journal_name

Proc Natl Acad Sci U S A

journal_title

Proceedings of the National Academy of Sciences of the United States of America

authors

Yu JJ,Robb VA,Morrison TA,Ariazi EA,Karbowniczek M,Astrinidis A,Wang C,Hernandez-Cuebas L,Seeholzer LF,Nicolas E,Hensley H,Jordan VC,Walker CL,Henske EP

doi

10.1073/pnas.0810790106

subject

Has Abstract

pub_date

2009-02-24 00:00:00

pages

2635-40

issue

8

eissn

0027-8424

issn

1091-6490

pii

0810790106

journal_volume

106

pub_type

杂志文章

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