Estrogen activates pyruvate kinase M2 and increases the growth of TSC2-deficient cells
Identifieur interne : 000159 ( Main/Exploration ); précédent : 000158; suivant : 000160Estrogen activates pyruvate kinase M2 and increases the growth of TSC2-deficient cells
Auteurs : Yiyang Lu [États-Unis] ; Xiaolei Liu [États-Unis] ; Erik Zhang [États-Unis] ; Elizabeth J. Kopras [États-Unis] ; Eric P. Smith [États-Unis] ; Aristotelis Astreinidis [États-Unis] ; Chenggang Li [États-Unis, République populaire de Chine] ; Yuet-Kin Leung [États-Unis] ; Shuk-Mei Ho [États-Unis] ; Jane J. Yu [États-Unis]Source :
- PLoS ONE [ 1932-6203 ] ; 2020.
Abstract
Lymphangioleiomyomatosis (LAM) is a devastating lung disease caused by inactivating gene mutations in either
Url:
DOI: 10.1371/journal.pone.0228894
PubMed: 32078667
PubMed Central: 7032738
Affiliations:
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<front><div type="abstract" xml:lang="en"><p>Lymphangioleiomyomatosis (LAM) is a devastating lung disease caused by inactivating gene mutations in either <italic>TSC1</italic>
or <italic>TSC2</italic>
that result in hyperactivation of the mechanistic target of rapamycin complex 1 (mTORC1). As LAM occurs predominantly in women during their reproductive age and is exacerbated by pregnancy, the female hormonal environment, and in particular estrogen, is implicated in LAM pathogenesis and progression. However, detailed underlying molecular mechanisms are not well understood. In this study, utilizing human pulmonary LAM specimens and cell culture models of TSC2-deficient LAM patient-derived and rat uterine leiomyoma-derived cells, we tested the hypothesis that estrogen promotes the growth of mTORC1-hyperactive cells through pyruvate kinase M2 (PKM2). Estrogen increased the phosphorylation of PKM2 at Ser37 and induced the nuclear translocation of phospho-PKM2. The estrogen receptor antagonist Faslodex reversed these effects. Restoration of TSC2 inhibited the phosphorylation of PKM2 in an mTORC1 inhibitor-insensitive manner. Finally, accumulation of phosphorylated PKM2 was evident in pulmonary nodule from LAM patients. Together, our data suggest that female predominance of LAM might be at least in part attributed to estrogen stimulation of PKM2-mediated cellular metabolic alterations. Targeting metabolic regulators of PKM2 might have therapeutic benefits for women with LAM and other female-specific neoplasms.</p>
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