NEDD4 controls the expression of GUCD1, a protein upregulated in proliferating liver cells

Bellet, Marina Maria; Piobbico, Danilo; Bartoli, D.; Castelli, Marilena; Pieroni, Stefania; Brunacci, Cinzia; Chiacchiaretta, Martina; Sordo, Rachele Del; Fallarino, Francesca; Sidoni, Angelo; Puccetti, Paolo; Romani, Luigina; Servillo, Giuseppe; Fazia, Maria Agnese Della

doi:10.4161/cc.28760

Cited by 28 publications

(28 citation statements)

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“…To identify genes that are highly expressed and might play a prominent role along liver regeneration, a cDNA library from rat regenerating liver was constructed and screened by Bellet et al 3 Genes strongly associated with liver proliferation were successfully identified. Among them, the authors characterized a highly conserved and ubiquitously expressed gene, guanylyl cyclase domain containing 1 (GUCD1) 3 .…”

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confidence: 99%

“…Among them, the authors characterized a highly conserved and ubiquitously expressed gene, guanylyl cyclase domain containing 1 (GUCD1) 3 . Noticeably, the levels of GUCD1 mRNA were found to peak 2 h after partial hepatectomy, when immediate early genes are upregulated, and between 24 and 72 h, corresponding to the hepatocyte proliferative phase, suggesting that GUCD1 might play an important role in hepatocyte proliferation.…”

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confidence: 99%

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Liver proliferation: The GUCD1/NEDD4–1 connection

Calvisi

2014

Cell Cycle

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Liver proliferation: The GUCD1/NEDD4–1 connection

Calvisi

2014

Cell Cycle

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“…Stable cell lines were selected via the addiction of geneticin (0.4 mg/ml) (Sigma-Aldrich, St. Louis, MO, USA) to culture medium. Cell growth rates were determined as previously described (37). Briefly, H1299-and A549-INSL4 and relative control cells were seeded at a concentration of 1.5 × 10 5 cells/well.…”

Section: Discussionmentioning

confidence: 99%

Epigenetic control of INSL4 promotes cell growth and invasiveness in Non-Small-Cell Lung Cancer

Scopetti

Piobbico

Brunacci

et al. 2020

Preprint

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Background Non-Small Cell Lung Cancer accounts for 80–85% of all forms of Lung Cancer as leading cause of cancer-related death in human. Despite remarkable advances in the diagnosis and therapy of Lung Cancer, no significant improvements have thus far been achieved in terms of patients’ prognosis. Here, we investigated the role of INSL4 – a member of the relaxin family –in NSCLC.Methods We permanently overexpressed INSL4 in NSCLC cells in vitro to analyse the growth rate and the tumourigenic features. We further investigated the signalling pathways engaged in INSL4 overexpressing cells and the tumour growth ability by studying the tumour development in a patient derived tumour xenograft mouse model. Results We found a cell growth promoting effect by INSL4 overexpression in vitro in H1299 cells and in vivo in NOD/SCID mice. Surprisingly, in NSCLC-A549 cells, stable INSL4 overexpression has not showed similar effect, despite has an INSL4-mRNA expressed up to 22.000 fold more respect H1299. The INSL4-mRNA analysis of eight different NSCLC-derived cell lines, has revealed a great discrepancy between the amount of INSL4-mRNA and specific protein. Notably, similar result has been observed in studied NSCLC patients analysing and comparing INSL4 mRNA and protein expression. However, in a cohort of NSCLC patients, we found a significant inverse correlation between INSL4 expression and Overall Survival.Conclusions By combining the results from the in vitro and in vivo models and in silico analysis in patients whose NSCLCs adenocarcinoma spontaneously expressed high levels of INSL4 our results suggest that epigenetic modifications that affect INSL4 does not allow to assess precision therapy in selected patients without consider protein INSL4 amount.

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“…RNA extraction and qPCR were performed as previously described [48,49]. cDNA was reversetranscribed from 1µg of RNA using the iScript kit (Bio Rad,).…”

Section: Quantitative Real-time Polymerase Chain Reactionmentioning

confidence: 99%

Role of IL-17RA in the proliferative priming of hepatocytes in liver regeneration

et al. 2018

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A tight link has been established between inflammation and cancer. Liver regeneration is a widely used model to study the correlation between inflammation and proliferation. IL-6 is essentially involved in liver regeneration and in cancer. Recently, IL-17A has been shown to regulate not only inflammation, but also cell proliferation. Here, we analyze the role played by IL-17A signaling in liver regeneration by comparing cell proliferation in Wild Type and IL-17RA −/− mice. Partial hepatectomy experiments performed in IL-17RA −/− mice showed a delay in expression of earlygenes to prime the residual hepatocyte to proliferate, with subsequent delay in G 1 /S-phase transition. We demonstrated that IL-17RA regulates, by recruitment of non-parenchymal cell, the expression of IL-6, which in turn triggers the proliferation of residual hepatocytes. Our data indicate an important role played by IL-17RA in liver proliferation via IL-6. ARTICLE HISTORY

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NEDD4 controls the expression of GUCD1, a protein upregulated in proliferating liver cells

Cited by 28 publications

References 34 publications

Liver proliferation: The GUCD1/NEDD4–1 connection

Liver proliferation: The GUCD1/NEDD4–1 connection

Epigenetic control of INSL4 promotes cell growth and invasiveness in Non-Small-Cell Lung Cancer

Role of IL-17RA in the proliferative priming of hepatocytes in liver regeneration

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