Phosphorylation of 14-3-3ζ links YAP transcriptional activation to hypoxic glycolysis for tumorigenesis

Jia, Yu; Li, Huiyan; Wang, Jue; Wang, Ying; Zhang, Peng; Ma, Ning; Mo, Shi-Jing

doi:10.1038/s41389-019-0143-1

Cited by 27 publications

(45 citation statements)

References 47 publications

(56 reference statements)

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“…Interestingly, YAP cooperates with other transcription regulators to control many genes related to glycolysis. For example, YAP interacts with HIF1α and regulates the transcription of various genes involved in aerobic glycolysis such as GLUT1, HK2, ALDOA, LDHA, and PKM2 (129,130). The YAP-TEAD complex interacts with p65 and upregulates the transcription of HK2 (131).…”

Section: The Role Of Yap/taz In Glucose Metabolismmentioning

confidence: 99%

A Potential Role of YAP/TAZ in the Interplay Between Metastasis and Metabolic Alterations

Yamaguchi

Taouk

2020

Front. Oncol.

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Yes-Associated Protein (YAP) and Transcriptional Co-activator with PDZ-binding Motif (TAZ) are the downstream effectors of the Hippo signaling pathway that play a crucial role in various aspects of cancer progression including metastasis. Metastasis is the multistep process of disseminating cancer cells in a body and responsible for the majority of cancer-related death. Emerging evidence has shown that cancer cells reprogram their metabolism to gain proliferation, invasion, migration, and anti-apoptotic abilities and adapt to various environment during metastasis. Moreover, it has increasingly been recognized that YAP/TAZ regulates cellular metabolism that is associated with the phenotypic changes, and recent studies suggest that the YAP/TAZ-mediated metabolic alterations contribute to metastasis. In this review, we will introduce the latest knowledge of YAP/TAZ regulation and function in cancer metastasis and metabolism, and discuss possible links between the YAP/TAZ-mediated metabolic reprogramming and metastasis.

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Section: The Role Of Yap/taz In Glucose Metabolismmentioning

confidence: 99%

A Potential Role of YAP/TAZ in the Interplay Between Metastasis and Metabolic Alterations

Yamaguchi

Taouk

2020

Front. Oncol.

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“…Hypoxia-inducible factor 1α (HIF1α) and c-Myc as the main transcription factors regulating glycolysis [62,63] were also found to be associated with YAP and to regulate the expression of key glycolysis enzymes and glycolysis. As studies reported, YAP binds to these transcription factors in the nucleus and regulates cell glycolysis [62,[64][65][66]. Altogether, Hippo signaling can regulate cell glucose metabolism in a variety of ways.…”

Section: Regulation Of Metabolism By Hippo Signalingmentioning

confidence: 87%

The Hippo Pathway: A Master Regulatory Network Important in Cancer

Liu

Song

2021

Cells

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The Hippo pathway is pervasively activated and has been well recognized to play critical roles in human cancer. The deregulation of Hippo signaling involved in cancer development, progression, and resistance to cancer treatment have been confirmed in several human cancers. Its biological significance and deregulation in cancer have drawn increasing interest in the past few years. A fundamental understanding of the complexity of the Hippo pathway in cancer is crucial for improving future clinical interventions and therapy for cancers. In this review, we try to clarify the complex regulation and function of the Hippo signaling network in cancer development, including its role in signal transduction, metabolic regulation, and tumor development, as well as tumor therapies targeting the Hippo pathway.

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“…Furthermore, they are also involved in biological processes such as apoptosis [30], autophagy [31], EMT [32] and even the Warburg Effect [33]. For instance, in a hypoxic microenvironment, a noticeable link has been found between YAP transcriptional activation and hypoxic glycolysis governed by the ERK2-dependent 14-3-3ζ Ser37 [34]. The phosphorylation for malignant progression in MEK1/2 activates human ERK1/2 by rst catalysing the phosphorylation of Y204/187 and then T202/185, both residues of which occur within the activation segment.…”

Section: Discussionmentioning

confidence: 99%

A novel long non-coding RNA GK-IT1 promotes the carcinogenesis and progression of esophageal squamous cell carcinoma via mediating the phosphorylation of MAPK1

Yang

Zeng

Liu

et al. 2020

Preprint

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Background: Recent studies have shown that Long non-coding RNAs (lncRNAs) are crucial in the invasion, angiogenesis, progression, and metastasis of esophageal squamous cell carcinoma (ESCC). However, the biological functions and potential molecular mechanism of LncRNA GK-IT1 in esophageal squamous cell carcinoma has not been reported.Methods: We analysed the expression of GK-IT1 in ESCC and their adjacent normal tissues in the TCGA database. The quantitative real-time-PCR (qRT-PCR) was used to detect the expression of GK-IT1 in Clinical specimens. The Kaplan-Meier method was employed to draw the survival curve and then the statistical significance was calculated using the logarithmic rank test. a range of functional experiments in vivo and in vitro were used to explore the role of GK-IT1 in the carcinogenesis and development of ESCC. RNA pull down assay, RNA immunoprecipitation (RIP), fluorescence in situ hybridisation (FISH), agarose gel electrophoresis and immunofluorescence were all employed to explore the interaction mechanism between GK-IT1 and MAPK1 (mitogen activated protein kinase 1).Results: The expression of GK-IT1 was higher in ESCC than adjacent normal tissues, which was positively correlated with the clinical stage and shorter survival time. The knockout of the GK-IT1 gene significantly attenuated the abilities of ESCC cell proliferation, invasion and migration, induced apoptosis and autophagy in ESCC cells and inhibited tumour growth and tumour metastasis in vivo. on the contrary, the upregulation of GK-IT1 had the opposite effect. Further studies have shown that GK-IT1 can regulate the biological process of ESCC by regulating the phosphorylation of MAPK1.Conclusion: Our study reveals that GK-IT1 mediated the phosphorylation of MAPK1 improve the carcinogenesis and development of esophageal squamous cell carcinoma through ERK/MAPK pathway which indicates that GK-IT1 possesses substantial potential as a novel biomarker for ESCC prognosis and therapy.

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Phosphorylation of 14-3-3ζ links YAP transcriptional activation to hypoxic glycolysis for tumorigenesis

Cited by 27 publications

References 47 publications

A Potential Role of YAP/TAZ in the Interplay Between Metastasis and Metabolic Alterations

A Potential Role of YAP/TAZ in the Interplay Between Metastasis and Metabolic Alterations

The Hippo Pathway: A Master Regulatory Network Important in Cancer

A novel long non-coding RNA GK-IT1 promotes the carcinogenesis and progression of esophageal squamous cell carcinoma via mediating the phosphorylation of MAPK1

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