Ubiquitination‑deubiquitination in the Hippo signaling pathway (Review)

Liu, Yanting; Deng, Jun

doi:10.3892/or.2019.6956

Cited by 13 publications

(14 citation statements)

References 224 publications

(271 reference statements)

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“…e.g. requiring autophagy [35]. YAP is an oncogene that enhances transcription of genes involved in cell proliferation by partnering with TEAD family of transcription factors; thus, inactivation of YAP promotes cell death [36].…”

Section: Discussionmentioning

confidence: 99%

Neratinib inhibits Hippo/YAP signaling, reduces mutant K-RAS expression, and kills pancreatic and blood cancer cells

et al. 2019

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Prior studies demonstrated that the irreversible ERBB1/2/4 inhibitor neratinib caused plasma membrane-associated mutant K-RAS to localize in intracellular vesicles, concomitant with its degradation. Herein, we discovered that neratinib interacted with the chemically distinct irreversible ERBB1/2/4 inhibitor afatinib to reduce expression of ERBB1, ERBB2, K-RAS and N-RAS; this was associated with greater-than-additive cell killing of pancreatic tumor cells. Knock down of Beclin1, ATG16L1, Rubicon or cathepsin B significantly lowered the ability of neratinib to reduce ERBB1 and K-RAS expression, and to cause tumor cell death. Knock down of ATM-AMPK suppressed vesicle formation and knock down of cathepsin B-AIF significantly reduced neratinib lethality. PKG phosphorylates K-RAS and HMG CoA reductase inhibitors reduce K-RAS farnesylation both of which remove K-RAS from the plasma membrane, abolishing its activity. Neratinib interacted with the PKG activator sildenafil and the HMG CoA reductase inhibitor atorvastatin to further reduce K-RAS expression, and to further enhance cell killing. Neratinib is also a Ste20 kinase family inhibitor and in carcinoma cells, and hematopoietic cancer cells lacking ERBB1/2/4, it reduced K-RAS expression and the phosphorylation of MST1/3/4/ Ezrin by ~30%. Neratinib increased LATS1 phosphorylation as well as that of YAP and TAZ also by ~30%, caused the majority of YAP to translocate into the cytosol and reduced YAP/TAZ #

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Section: Discussionmentioning

confidence: 99%

Neratinib inhibits Hippo/YAP signaling, reduces mutant K-RAS expression, and kills pancreatic and blood cancer cells

et al. 2019

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“…No connection in the literature have been made between this proteotoxicity-induced ferroptosis and cell-to-cell contact, but it is worth noting that the activity of Hippo pathway depends largely on ubiquitination-deubiquitination status (review in ref. 120 ). Namely, the activities of Hippo pathway components, including YAP/TAZ regulators, are under direct regulation of ubiquitination-deubiquitination process.…”

Section: Hippo Pathway and Proteotoxic Stressmentioning

confidence: 99%

Together we stand, apart we fall: how cell-to-cell contact/interplay provides resistance to ferroptosis

et al. 2020

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Contextualisation of the new type of cell death called “ferroptosis” opened a completely new avenue for the development of anti-cancer therapies. Cumulative fundamental research dating back to the mid-20th century, crowned by the extraordinary work of the group led by Dr. Stockwell from Columbia University in 2012, finally got its candidature to be applied in the clinical settings. Although the potential for clinical importance is undoubtedly growing every day, as showed by the increasing number of papers dealing with ferroptosis and its applications, long experience of cancer research and treatment taught us that caution is still necessary. The plasticity of the tumour cells, particularly acute, along with its involvement in the resistance mechanisms, that have been seen, to greater or lesser extent, for almost all currently used therapies, represents the biggest fascinations in biomedical research field and also the biggest challenge to achieving cures in cancer patients. Accordingly, the main features of fundamental research have to be vigilance and anticipation. In this review, we tried to summarize the literature data, accumulated in the past couple of years, which point out the pitfalls in which “ferroptosis inducers” can fall if used prematurely in the clinical settings, but at the same time can provide a great advantage in the exhausting battle with cancer resistance. This is the first comprehensive review focusing on the effects of the cell-to-cell contact/interplay in the development of resistance to ferroptosis, while the contribution of cell-born factors has been summarized previously so here we just listed them.

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“…35,36 In addition to the autophagy lysosomal degradation pathway, YAP is primarily degraded through the ubiquitin proteasome pathway by recruiting the E3 ubiquitin ligases SCF b-TRCP , FBXW7, and SOCS5/6. 35,50,51 Our results demonstrated that SPTBN1 reduced protein levels of LATS1 and YAP and increased levels of p-LATS1 and p-YAP S127 , leading to decreased YAP nuclear localization in Huh-7 and PLC/PRF/5 HCC cells. Furthermore, MG132 enhanced the increase of YAP/ p-YAP S127 caused by SPTBN1 knockdown, indicating that loss of SPTBN1 promoted total YAP stabilization by decreasing proteasome degradation.…”

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confidence: 59%

Loss of SPTBN1 Suppresses Autophagy Via SETD7-mediated YAP Methylation in Hepatocellular Carcinoma Initiation and Development

Chen

Wang

et al. 2022

Cellular and Molecular Gastroenterology and Hepatology

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Spectrin beta, non-erythrocytic 1 cooperates with suppressor of variegation 3-9-enhancer of zeste-trithorax domain containing lysine methyltransferase 7 to promote Yesassociated protein methylation, enhancing autophagy of hepatic stem cells, hepatocellular carcinoma cells, and hepatocytes. Loss of spectrin beta, non-erythrocytic 1 promotes expansion and malignant transformation of hepatic stem cells via inhibiting autophagy during hepatocarcinogenesis.

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Ubiquitination‑deubiquitination in the Hippo signaling pathway (Review)

Cited by 13 publications

References 224 publications

Neratinib inhibits Hippo/YAP signaling, reduces mutant K-RAS expression, and kills pancreatic and blood cancer cells

Neratinib inhibits Hippo/YAP signaling, reduces mutant K-RAS expression, and kills pancreatic and blood cancer cells

Together we stand, apart we fall: how cell-to-cell contact/interplay provides resistance to ferroptosis

Loss of SPTBN1 Suppresses Autophagy Via SETD7-mediated YAP Methylation in Hepatocellular Carcinoma Initiation and Development

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