scholarly journals Gastrin-Releasing Peptide-Induced Down-Regulation of Tumor Suppressor Protein PTEN (Phosphatase and Tensin Homolog Deleted on Chromosome Ten) in Neuroblastomas

2005 ◽  
Vol 241 (5) ◽  
pp. 684-692 ◽  
Author(s):  
Jingbo Qiao ◽  
Junghee Kang ◽  
Jeremy Cree ◽  
B Mark Evers ◽  
Dai H. Chung
Keyword(s):  
Tumor Suppressor ◽  
Tumor Suppressor Protein ◽  
Down Regulation ◽  
Phosphatase And Tensin Homolog ◽  
Gastrin Releasing Peptide ◽  
Tensin Homolog

Familial Intracranial Hypertension in 2 Brothers WithPTENMutation: Expansion of the Phenotypic Spectrum

2019 ◽  
Vol 34 (9) ◽  
pp. 506-510 ◽  
Author(s):  
Ronen Hady-Cohen ◽  
Idit Maharshak ◽  
Marina Michelson ◽  
Keren Yosovich ◽  
Dorit Lev ◽  
...  
Keyword(s):  
Intracranial Pressure ◽  
Tumor Suppressor ◽  
Intracranial Hypertension ◽  
Signaling Pathway ◽  
Clinical Presentation ◽  
Tumor Suppressor Protein ◽  
Phosphatase And Tensin Homolog ◽  
Tensin Homolog ◽  
Phenotypic Spectrum ◽  
Wide Variability

PTEN (Phosphatase and Tensin Homolog on chromosome TEN) encodes a vastly expressed tumor suppressor protein that antagonizes the PI3 K signaling pathway and alters the MTOR pathway. Mutations in PTEN have been described in association with a number of syndromes including PTEN hamartoma-tumor syndrome, macrocephaly/autism, and juvenile polyposis of infancy. Although there is a wide variability in the clinical and radiologic presentations of PTEN-related phenotypes, the most consistent features include macrocephaly and increased tumorigenesis. Intracranial hypertension may be idiopathic or secondary to multiple etiologies. We describe 2 siblings harboring a PTEN mutation who presented with macrocephaly and intracranial hypertension. Repeat brain MRIs were normal in both. Acetazolamide treatment normalized intracranial pressure, but several trials of medication tapering led to recurrence of intracranial hypertension symptoms. The clinical presentation of our patients expands the PTEN-related phenotypes. We discuss the possible pathophysiology in view of PTEN function.

Down-regulation of phosphatase and tensin homolog by hepatitis C virus core 3a in hepatocytes triggers the formation of large lipid droplets

Hepatology ◽  
2011 ◽  
Vol 54 (1) ◽  
pp. 38-49 ◽  
Author(s):  
Sophie Clément ◽  
Marion Peyrou ◽  
Andrea Sanchez-Pareja ◽  
Lucie Bourgoin ◽  
Pierluigi Ramadori ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Lipid Droplets ◽  
Down Regulation ◽  
Phosphatase And Tensin Homolog ◽  
Tensin Homolog ◽  
Virus Core

scholarly journals Phosphatase and Tensin Homolog in Non-neoplastic Digestive Disease: More Than Just Tumor Suppressor

2021 ◽  
Vol 12 ◽  
Author(s):  
Tianyu He ◽  
Xiaoyun Zhang ◽  
Jianyu Hao ◽  
Shigang Ding
Keyword(s):  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Malignant Tumors ◽  
Biological Effects ◽  
Pten Protein ◽  
Phosphatase And Tensin Homolog ◽  
Tensin Homolog ◽  
Lipid Phosphatase ◽  
And Migration

The Phosphatase and tensin homolog (PTEN) gene is one of the most important tumor suppressor genes, which acts through its unique protein phosphatase and lipid phosphatase activity. PTEN protein is widely distributed and exhibits complex biological functions and regulatory modes. It is involved in the regulation of cell morphology, proliferation, differentiation, adhesion, and migration through a variety of signaling pathways. The role of PTEN in malignant tumors of the digestive system is well documented. Recent studies have indicated that PTEN may be closely related to many other benign processes in digestive organs. Emerging evidence suggests that PTEN is a potential therapeutic target in the context of several non-neoplastic diseases of the digestive tract. The recent discovery of PTEN isoforms is expected to help unravel more biological effects of PTEN in non-neoplastic digestive diseases.

scholarly journals Unsaturated fatty acids inhibit the expression of tumor suppressor phosphatase and tensin homolog (PTEN) via microRNA-21 up-regulation in hepatocytes

Hepatology ◽  
2008 ◽  
Vol 49 (4) ◽  
pp. 1176-1184 ◽  
Author(s):  
Manlio Vinciguerra ◽  
Antonino Sgroi ◽  
Christelle Veyrat-Durebex ◽  
Laura Rubbia-Brandt ◽  
Leo H. Buhler ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Tumor Suppressor ◽  
Unsaturated Fatty Acids ◽  
Phosphatase And Tensin Homolog ◽  
Tensin Homolog

scholarly journals PTENSequence Analysis in Endometrial Hyperplasia and Endometrial Carcinoma in Slovak Women

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
H. Gbelcová ◽  
P. Bakeš ◽  
P. Priščáková ◽  
V. Šišovský ◽  
I. Hojsíková ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Endometrial Carcinoma ◽  
Endometrial Hyperplasia ◽  
Female Genital Tract ◽  
Suppressor Gene ◽  
Serous Carcinoma ◽  
Tissue Samples ◽  
Phosphatase And Tensin Homolog ◽  
Coding Regions ◽  
Tensin Homolog

Phosphatase and tensin homolog (PTEN) is a protein that acts as a tumor suppressor by dephosphorylating the lipid second messenger phosphatidylinositol 3,4,5-trisphosphate. Loss of PTEN function has been implicated in the pathogenesis of a number of different tumors, particularly endometrial carcinoma (ECa). ECa is the most common neoplasia of the female genital tract. Our study evaluates an association between the morphological appearance of endometrial hyperplasia and endometrial carcinoma and the degree ofPTENalterations. A total of 45 endometrial biopsies from Slovak women were included in present study. Formalin-fixed and paraffin-embedded tissue samples with simple hyperplasia (3), complex hyperplasia (5), atypical complex hyperplasia (7), endometrioid carcinomas G1 (20) and G3 (5), and serous carcinoma (5) were evaluated for the presence of mutations in coding regions ofPTENgene, the most frequently mutated tumor suppressor gene in endometrial carcinoma. 75% of the detected mutations were clustered in exons 5 and 8. Out of the 39 mutations detected in 24 cases, 20 were frameshifts and 19 were nonsense, missense, or silent mutations. Some specimens harboured more than one mutation. The results of current study on Slovak women were compared to a previous study performed on Polish population. The two sets of results were similar.

scholarly journals Role of Rap1B and Tumor Suppressor PTEN in the Negative Regulation of Lysophosphatidic Acid—induced Migration by Isoproterenol in Glioma Cells

2009 ◽  
Vol 20 (24) ◽  
pp. 5156-5165 ◽  
Author(s):  
Enkhzol Malchinkhuu ◽  
Koichi Sato ◽  
Tomohiko Maehama ◽  
Shogo Ishiuchi ◽  
Yuhei Yoshimoto ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Lysophosphatidic Acid ◽  
Adrenergic Receptor ◽  
Glioma Cells ◽  
Negative Regulation ◽  
Dominant Negative ◽  
Down Regulation ◽  
Small Interference Rna ◽  
Tensin Homolog ◽  
Invasive Behavior

The clarification of mechanisms that negatively regulate the invasive behavior of human glioma cells is of great importance in order to find new methods of treatment. In this study, we have focused on the negative regulation of lysophosphatidic acid (LPA)-induced migration in glioma cells. Using small interference RNA and dominant-negative gene strategies in addition to pharmacological tools, we found that isoproterenol (ISO) and sphingosine-1-phosphate (S1P) negatively but differently regulate the LPA-induced migration. ISO-induced suppression of the migration of glioma cells occurs via β2-adrenergic receptor/cAMP/Epac/Rap1B/inhibition of Rac, whereas S1P has been shown to suppress the migration of the cells through S1P2 receptor/Rho-mediated down-regulation of Rac1. The expression of tumor suppressor phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is required for the inhibitory ISO-induced and Rap1B-mediated actions on the migration, Rac1 activation, and Akt activation in response to LPA. Thus, the PTEN-mediated down-regulation of phosphatidylinositol 3-kinase activity may be involved in the regulation of Rap1B-dependent inhibition of Rac1 activity. These findings suggest that there are at least two distinct inhibitory pathways, which are mediated by the S1P2 receptor and β2-adrenergic receptor, to control the migratory, hence invasive, behavior of glioma cells.

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