O-GlcNAcylation: An Emerging Protein Modification Regulating the Hippo Pathway

The balance between cellular proliferation and apoptosis and the regulation of cell differentiation must be established to maintain tissue homeostasis. These cellular responses involve the kinase cascade-mediated Hippo pathway as a crucial regulator. Hence, Hippo pathway dysregulation is implicated...

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Bibliographic Details
Published in:Cancers 2022-06, Vol.14 (12), p.3013
Main Authors: Kim, Eunah, Kang, Jeong Gu, Jho, Eek-hoon, Yang, Won Ho, Cho, Jin Won
Format: Article
Language:English
Subjects:
Adapter proteins
Apoptosis
Cancer
Cell differentiation
Cytoplasm
Enzymes
Feedback
Gene expression
Glucose
Glycosylation
Homeostasis
Hyperplasia
Kinases
Metastasis
O-GlcNAcylation
Phosphorylation
Review
Signal transduction
Tumorigenesis
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Summary:The balance between cellular proliferation and apoptosis and the regulation of cell differentiation must be established to maintain tissue homeostasis. These cellular responses involve the kinase cascade-mediated Hippo pathway as a crucial regulator. Hence, Hippo pathway dysregulation is implicated in diverse diseases, including cancer. O-GlcNAcylation is a non-canonical glycosylation that affects multiple signaling pathways through its interplay with phosphorylation in the nucleus and cytoplasm. An abnormal increase in the O-GlcNAcylation levels in various cancer cells is a potent factor in Hippo pathway dysregulation. Intriguingly, Hippo pathway dysregulation also disrupts O-GlcNAc homeostasis, leading to a persistent elevation of O-GlcNAcylation levels, which is potentially pathogenic in several diseases. Therefore, O-GlcNAcylation is gaining attention as a protein modification that regulates the Hippo pathway. This review presents a framework on how O-GlcNAcylation regulates the Hippo pathway and forms a self-perpetuating cycle with it. The pathological significance of this self-perpetuating cycle and clinical strategies for targeting O-GlcNAcylation that causes Hippo pathway dysregulation are also discussed.
ISSN:2072-6694
2072-6694
DOI:10.3390/cancers14123013