Yin Yang 1 and raf-1 Kinase Inhibitory Protein Status in Hepatocellular carcinoma: Future Perspectives

2010 ◽  
Vol 1 (1-2) ◽  
pp. 97-114
Author(s):  
Natale D'Alessandro ◽  
Lydia Giannitrapani ◽  
Manuela Labbozzetta ◽  
Paola Poma ◽  
Luigi Inguglia ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Future Perspectives ◽  
Inhibitory Protein ◽  
Protein Status ◽  
Yin Yang 1 ◽  
Yin Yang

T.N.20 ALTERED YIN YANG 1/RAF-1 KINASE INHIBITORY PROTEIN RATIO AS A POSSIBLE MOLECULAR MARKER AND THERAPEUTIC TARGET IN HEPATOCELLULAR CARCINOMA

2010 ◽  
Vol 42 ◽  
pp. S22
Author(s):  
M. Notarbartolo ◽  
L. Giannitrapani ◽  
P. Poma ◽  
M. Labbozzetta ◽  
A.M. Florena ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Molecular Marker ◽  
Therapeutic Target ◽  
Inhibitory Protein ◽  
Protein Ratio ◽  
Yin Yang 1 ◽  
Yin Yang

Frequent Alteration of the Yin Yang 1/Raf-1 Kinase Inhibitory Protein Ratio in Hepatocellular Carcinoma

2011 ◽  
Vol 15 (5) ◽  
pp. 267-272 ◽  
Author(s):  
Monica Notarbartolo ◽  
Lydia Giannitrapani ◽  
Nicoletta Vivona ◽  
Paola Poma ◽  
Manuela Labbozzetta ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Inhibitory Protein ◽  
Protein Ratio ◽  
Yin Yang 1 ◽  
Yin Yang

Yin Yang 1-mediated epigenetic silencing of tumour-suppressive microRNAs activates nuclear factor-κB in hepatocellular carcinoma

2016 ◽  
Vol 238 (5) ◽  
pp. 651-664 ◽  
Author(s):  
Daisy PF Tsang ◽  
William KK Wu ◽  
Wei Kang ◽  
Ying-Ying Lee ◽  
Feng Wu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Nuclear Factor Κb ◽  
Epigenetic Silencing ◽  
Nuclear Factor ◽  
Yin Yang 1 ◽  
Yin Yang

scholarly journals The pattern of gene copy number variations (CNVs) in hepatocellular carcinoma; in silico analysis

2021 ◽  
Author(s):  
Arman Shahrisa ◽  
Maryam Tahmaseby ◽  
Hossein Ansari ◽  
Zahra Mohammadi ◽  
Vinicio Carloni ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Suppressor ◽  
In Silico ◽  
Tumor Suppressor Genes ◽  
Copy Number ◽  
Gene Copy ◽  
Suppressor Genes ◽  
Body Protein ◽  
Yin Yang 1 ◽  
Yin Yang

Abstract Recent studies showed that genetic lost or gain in the genome can predispose cells toward malignancy. Hepatocellular carcinoma (HCC) is the most common type of liver cancer which occurs predominantly in patients with underlying chronic liver disease and cirrhosis. Prognosis of HCC is strongly connected with diagnostic delay. To date, no ideal screening modality has been developed for HCC. Recent findings demonstrated that Copy number variation (CNVs) can lead to activation of oncogenes and inactivation of tumor suppressor genes in cancers. In this study, CNV profile of 361 HCC samples was evaluated to reveal the potent - chromosomal regions involved in the disease. The obtained data showed that the chr1q and chr8p were two hotspot regions for gene amplifications and deletions in studied samples respectively. In this research, YY1AP1 (Yin Yang-1 Associated Protein 1) on chr1q22 was the most amplified gene in HCC samples and showed the positive correlation with tumor grade. Deletion of CHMP7 (Charged Multivesicular Body Protein 7) on chr8p21.3 was another frequently observed CNV among HCC patients. Both genes were interacted with variety of well-known oncogenes and tumor suppressor genes including YY1 (Yin Yang 1), CCND1 (Cyclin D1), HDAC1 (Histone deacetylase 1), VHL (von Hippel-Lindau tumor suppressor), MAD2L2 (Mitotic Arrest Deficient 2 Like 2), CEBPA (CCAAT/enhancer-binding protein alpha), CHMP4A, CHMP5, CHMP2A, CHMP3 and ENSG00000249884 (RNF103-CHMP3 gene), all of them are well-known in carcinogenesis. Although this study was based on in silico evaluations, our findings can open a new window for researchers of HCC to focus on such candidate genes during experimental assays.

Physical Interaction of Human Yin Yang 1 Protein with DNA

2017 ◽  
Vol 22 (1-2) ◽  
pp. 75-97 ◽  
Author(s):  
Małgorzata Figiel ◽  
Andrzej Górecki
Keyword(s):  
Physical Interaction ◽  
Yin Yang 1 ◽  
Yin Yang

scholarly journals Interplay Between Heme Oxygenase-1 and the Multifunctional Transcription Factor Yin Yang 1 in the Inhibition of Intimal Hyperplasia

2010 ◽  
Vol 107 (12) ◽  
pp. 1490-1497 ◽  
Author(s):  
Konstanze Beck ◽  
Ben J. Wu ◽  
Jun Ni ◽  
Fernando S. Santiago ◽  
Kristine P. Malabanan ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Heme Oxygenase ◽  
Intimal Hyperplasia ◽  
Heme Oxygenase 1 ◽  
Yin Yang 1 ◽  
Yin Yang ◽  
Multifunctional Transcription Factor

scholarly journals MicroRNA-122 Inhibits Lipid Droplet Formation and Hepatic Triglyceride Accumulation via Yin Yang 1

2017 ◽  
Vol 44 (4) ◽  
pp. 1651-1664 ◽  
Author(s):  
Guo-yi Wu ◽  
Chen Rui ◽  
Ji-qiao Chen ◽  
Eiketsu Sho ◽  
Shan-shan Zhan ◽  
...  
Keyword(s):  
Quantitative Pcr ◽  
Lipid Droplet ◽  
Droplet Formation ◽  
Luciferase Assay ◽  
Luciferase Reporter ◽  
Hepatic Triglyceride ◽  
Yin Yang 1 ◽  
Lipid Droplet Formation ◽  
Huh7 Cells ◽  
Yin Yang

Background/Aims: An increase in intracellular lipid droplet formation and hepatic triglyceride (TG) content usually results in nonalcoholic fatty liver disease. However, the mechanisms underlying the regulation of hepatic TG homeostasis remain unclear. Methods: Oil red O staining and TG measurement were performed to determine the lipid content. miRNA expression was evaluated by quantitative PCR. A luciferase assay was performed to validate the regulation of Yin Yang 1 (YY1) by microRNA (miR)-122. The effects of miR-122 expression on YY1 and its mechanisms involving the farnesoid X receptor and small heterodimer partner (FXR-SHP) pathway were evaluated by quantitative PCR and Western blot analyses. Results: miR-122 was downregulated in free fatty acid (FFA)-induced steatotic hepatocytes, and streptozotocin and high-fat diet (STZ-HFD) induced nonalcoholic steatohepatitis (NASH) in mice. Transfection of hepatocytes with miR-122 mimics before FFA induction inhibited lipid droplet formation and TG accumulation in vitro. These results were verified by overexpressing miR-122 in the livers of STZ-HFD-induced NASH mice. The 3’-untranslated region (3’UTR) of YY1 mRNA is predicted to contain an evolutionarily conserved miR-122 binding site. In silico searches, a luciferase reporter assay and quantitative PCR analysis confirmed that miR-122 directly bound to the YY1 3’UTR to negatively regulate YY1 mRNA in HepG2 and Huh7 cells. The (FXR-SHP) signaling axis, which is downstream of YY1, may play a key role in the mechanism of miR-122-regulated lipid homeostasis. YY1-FXR-SHP signaling, which is negatively regulated by FFA, was enhanced by miR-122 overexpression. This finding was also confirmed by overexpression of miR-122 in the livers of NASH mice. Conclusions: The present results indicate that miR-122 plays an important role in lipid (particularly TG) accumulation in the liver by reducing YY1 mRNA stability to upregulate FXR-SHP signaling.

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