ChloroquineV1, an2020, Analysis, bibRecord, 000159

Estrogen activates pyruvate kinase M2 and increases the growth of TSC2-deficient cells

Identifieur interne : 000159 ( an2020/Analysis ); précédent : 000158; suivant : 000160

Estrogen 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.

RBID : PMC:7032738

Abstract

Lymphangioleiomyomatosis (LAM) is a devastating lung disease caused by inactivating gene mutations in either TSC1 or TSC2 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.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7032738

DOI: 10.1371/journal.pone.0228894
PubMed: 32078667
PubMed Central: 7032738

Affiliations:

Links to Exploration step

PMC:7032738

Le document en format XML

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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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<affiliations><list><country><li>République populaire de Chine</li>
<li>États-Unis</li>
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</settlement>
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<name sortKey="Zhang, Erik" sort="Zhang, Erik" uniqKey="Zhang E" first="Erik" last="Zhang">Erik Zhang</name>
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<country name="République populaire de Chine"><noRegion><name sortKey="Li, Chenggang" sort="Li, Chenggang" uniqKey="Li C" first="Chenggang" last="Li">Chenggang Li</name>
</noRegion>
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   |wiki=    Sante
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   |flux=    an2020
   |étape=   Analysis
   |type=    RBID
   |clé=     PMC:7032738
   |texte=   Estrogen activates pyruvate kinase M2 and increases the growth of TSC2-deficient cells
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Serveur d'exploration Chloroquine

Estrogen activates pyruvate kinase M2 and increases the growth of TSC2-deficient cells

Estrogen activates pyruvate kinase M2 and increases the growth of TSC2-deficient cells

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	Serveur d'exploration Chloroquine
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