Cross-talk between YAP and RAR-RXR Drives Expression of Stemness Genes to Promote 5-FU Resistance and Self-Renewal in Colorectal Cancer Cells.


Journal

Molecular cancer research : MCR
ISSN: 1557-3125
Titre abrégé: Mol Cancer Res
Pays: United States
ID NLM: 101150042

Informations de publication

Date de publication:
04 2021
Historique:
received: 19 05 2020
revised: 10 11 2020
accepted: 12 01 2021
pubmed: 22 1 2021
medline: 13 1 2022
entrez: 21 1 2021
Statut: ppublish

Résumé

The mechanisms whereby the Hippo pathway effector YAP regulates cancer cell stemness, plasticity, and chemoresistance are not fully understood. We previously showed that in 5-fluorouracil (5-FU)-resistant colorectal cancer cells, the transcriptional coactivator YAP is differentially regulated at critical transitions connected with reversible quiescence/dormancy to promote metastasis. Here, we found that experimental YAP activation in 5-FU-sensitive and 5-FU-resistant HT29 colorectal cancer cells enhanced nuclear YAP localization and the transcript levels of the retinoic acid (RA) receptors RARα/γ and RAR target genes

Identifiants

pubmed: 33472949
pii: 1541-7786.MCR-20-0462
doi: 10.1158/1541-7786.MCR-20-0462
doi:

Substances chimiques

Cell Cycle Proteins 0
Receptors, Retinoic Acid 0
Retinoid X Receptors 0
Transcription Factors 0
YY1AP1 protein, human 0
Fluorouracil U3P01618RT

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

612-622

Informations de copyright

©2021 American Association for Cancer Research.

Références

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Auteurs

Marjolaine Bauzone (M)

Université Lille, CNRS, Inserm, CHU Lille, UMR9020-UMR1277 - CANTHER - Cancer Heterogeneity, Plasticity and Resistance to Therapies, Lille, France.

Mouloud Souidi (M)

Université Lille, CNRS, Inserm, CHU Lille, UMR9020-UMR1277 - CANTHER - Cancer Heterogeneity, Plasticity and Resistance to Therapies, Lille, France.

Anne-Frédérique Dessein (AF)

Université Lille, CNRS, Inserm, CHU Lille, UMR9020-UMR1277 - CANTHER - Cancer Heterogeneity, Plasticity and Resistance to Therapies, Lille, France.
Centre de Biopathologie, Lille CHU, Lille, France.

Maxence Wisztorski (M)

Université Lille, Inserm, CHU Lille, U1192 - Protéomique Réponse Inflammatoire Spectrométrie de Masse - PRISM, Lille, France.

Audrey Vincent (A)

Université Lille, CNRS, Inserm, CHU Lille, UMR9020-UMR1277 - CANTHER - Cancer Heterogeneity, Plasticity and Resistance to Therapies, Lille, France.

Jean-Pascal Gimeno (JP)

Université Lille, Inserm, CHU Lille, U1192 - Protéomique Réponse Inflammatoire Spectrométrie de Masse - PRISM, Lille, France.

Didier Monté (D)

CNRS ERL9002 Integrative Structural Biology, Lille, France.
Université Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1167 - RID-AGE - Risk Factors and Molecular Determinants of Aging-Related Diseases, Lille, France.

Isabelle Van Seuningen (I)

Université Lille, CNRS, Inserm, CHU Lille, UMR9020-UMR1277 - CANTHER - Cancer Heterogeneity, Plasticity and Resistance to Therapies, Lille, France.

Christian Gespach (C)

Sorbonne Université, Inserm U938, Team TGFβ Signaling in Cellular Plasticity and Cancer, Centre de Recherche Saint-Antoine, CRSA, Paris, France.

Guillemette Huet (G)

Université Lille, CNRS, Inserm, CHU Lille, UMR9020-UMR1277 - CANTHER - Cancer Heterogeneity, Plasticity and Resistance to Therapies, Lille, France. guillemette.huet@inserm.fr.
Centre de Biopathologie, Lille CHU, Lille, France.

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