scholarly journals Polymorphisms of cell cycle regulator genes CCND1 G870A and TP53 C215G: Association with colorectal cancer susceptibility risk in a Malaysian population

2015 ◽  
Vol 10 (5) ◽  
pp. 3216-3222 ◽  
Author(s):  
MOHD NIZAM ZAHARY ◽  
ABDUL AZIZ AHMAD AIZAT ◽  
GURJEET KAUR ◽  
LEE YEONG YEH ◽  
MAYA MAZUWIN ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Cancer Susceptibility ◽  
Malaysian Population ◽  
Cell Cycle Regulator ◽  
Regulator Genes ◽  
Ccnd1 G870a

Cell cycle analysis and expression of cell cycle regulator genes in myeloma cells overexpressing cyclin D1

2001 ◽  
Vol 114 (3) ◽  
pp. 591-599 ◽  
Author(s):  
Kenichiro Yata ◽  
Yoshito Sadahira ◽  
Takemi Otsuki ◽  
Haruko Sakaguchi ◽  
Yumika Isozaki ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cyclin D1 ◽  
Cell Cycle Analysis ◽  
Myeloma Cells ◽  
Cell Cycle Regulator ◽  
Regulator Genes

scholarly journals Aryl hydrocarbon receptor (AHR) is a potential tumour suppressor in pituitary adenomas

2017 ◽  
Vol 24 (8) ◽  
pp. 445-457 ◽  
Author(s):  
R Formosa ◽  
J Borg ◽  
J Vassallo
Keyword(s):  
Cell Cycle ◽  
Aryl Hydrocarbon Receptor ◽  
Pituitary Adenomas ◽  
Tumour Suppressor ◽  
Gh3 Cells ◽  
Altered Expression ◽  
Aryl Hydrocarbon ◽  
Cell Cycle Regulator ◽  
Regulator Genes

Pituitary adenomas (PA) represent the largest group of intracranial neoplasms and yet the molecular mechanisms driving this disease remain largely unknown. The aim of this study was to use a high-throughput screening method to identify molecular pathways that may be playing a significant and consistent role in PA. RNA profiling using microarrays on eight local PAs identified the aryl hydrocarbon receptor (AHR) signalling pathway as a key canonical pathway downregulated in all PA types. This was confirmed by real-time PCR in 31 tumours. The AHR has been shown to regulate cell cycle progression in various cell types; however, its role in pituitary tissue has never been investigated. In order to validate the role of AHR in PA behaviour, further functional studies were undertaken. Over-expression of AHR in GH3 cells revealed a tumour suppressor potential independent of exogenous ligand activation by benzo α-pyrene (BαP). Cell cycle analysis and quantitative PCR of cell cycle regulator genes revealed that both unstimulated and BαP-stimulated AHR reduced E2F-driven transcription and altered expression of cell cycle regulator genes, thus increasing the percentage of cells in G0/G1 phase and slowing the proliferation rate of GH3 cells. Co-immunoprecipitation confirmed the interaction between AHR and retinoblastoma (Rb1) protein supporting this as a functional mechanism for the observed reduction. Endogenous Ahr reduction using silencing RNA confirmed the tumour suppressive function of the Ahr. These data support a mechanistic pathway for the putative tumour suppressive role of AHR specifically in PA, possibly through its role as a cell cycle co-regulator, even in the absence of exogenous ligands.

Promoter hypermethylation profile of cell cycle regulator genes in pituitary adenomas

2007 ◽  
Vol 83 (2) ◽  
pp. 153-162 ◽  
Author(s):  
Atsuo Yoshino ◽  
Yoichi Katayama ◽  
Akiyoshi Ogino ◽  
Takao Watanabe ◽  
Kazunari Yachi ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Pituitary Adenomas ◽  
Promoter Hypermethylation ◽  
Cell Cycle Regulator ◽  
Regulator Genes

Changes of Megakaryocyte Gene Expression When Essential Thrombocythemia (ET) Transform Into Myelofibrosis (Post-ET MF) by Microarray Analysis,

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 3845-3845
Author(s):  
Hemant Sindhu ◽  
Chi Chen ◽  
Muhammad I. Kafeel ◽  
Yiwu Sun ◽  
Ching Wong ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Growth Factor ◽  
Microarray Analysis ◽  
Conflicts Of Interest ◽  
Expression Profiles ◽  
Growth Factor Receptor ◽  
Cell Cycle Regulator ◽  
Growth Factor Genes ◽  
Regulator Genes

Abstract Abstract 3845 Patients with ET eventually transform into Post- ET MF. The underlying mechanism of the transformation is still unknown. Megakaryocytes play an important role in the pathogenesis of bone marrow fibrosis in MF; ET and Post-ET MF also are characterized by abnormal megakaryocytic proliferation. Therefore we have performed microarray analysis of gene expression profiles to compare megakaryocytes derived from patients with Post-ET MF to ET. CD 34+ cells were obtained from peripheral blood, then cultured with Serum-Free Medium of stem cell factor (100 ng/mL) and thrombopoietin (TPO 100 ng/mL). Megakaryocytes (MK) were obtained by MACS selection of CD 61+ cells after 10 days culture. MK from two pooled ET-MF and a pooled from eight ET patients were extracted into RNA then converted to cDNA and amplified by PCR, followed by hybridization to an oligonucleotide microchip in PhalanxBio Inc. (Palo Alto, Ca). Gene expression levels in MK cells from ET-MF patients expressed in threshold cycle (CT) values were validated by statistical analysis of replicates and normalized to that from pooled ET patients to generate fold-change and statistical relevance. The resulting signal log ratios (SLRs) were used to classify the expressed genes into various groups according to its graded values. The results of post-ET MF compared with ET were as follows: 1) with analysis of 4544 genes, SLR <-1 were 6.58 %, and 10.12 % were >1, 2) in apoptosis genes, over expressed genes were IGF-1R, CFLAR, NFKBA,(GLR between 1–1.5) down-regulated genes were BAX, LGALSI, PPPIR 15A, CASP3 (GLR between -0.5 to -0.1), 3) in cell cycle controlling genes, over expressed were IL8, INSIG1, IGF-1R, BCL3(GLR between 1 to 1.5), down-regulated were PPPIR15A (GLR= -0.7). 4) in megakaryocyte-important development genes, growth factor genes including PDGF A, C were up-regulated (GLR=1.8), and VEG B was down-regulated (GLR= -1. 4):; growth factor receptor genes including IL1R 1and 2, CXCR4, IL8, PF4 were up-regulated (GLR between 1–2), IL3RA, KIT were down-regulated (GLR between -1.6 to -3); cell cycle regulator genes including CCND1, 3, RASGRP3 were up-regulated (GLR between 1 to 2.5), CDK4 was down-regulated (GLR = -1); transcription regulators including CEBPE, CEBPG were up-regulated (GLR-1.5); all Signal transducers including all STAT 1–5, MAK14 were up-regulated (GLR between 1.5 to 2.4). There are 20 up-regulated genes and 20 down-regulated genes which need further analysis for their function. These analyses of MK genes comparison between Post ET-MF and ET suggest that many anti-apoptosis, cell cycle regulator genes, growth factor genes, growth factor receptor genes and all of the signal transducer genes for the MK development genes were up-regulated while many of the pro-apoptosis genes were down-regulated. These gene changes found in the present study, when transformation of ET into post-ET MF occurs will be important for understanding this disease process and target therapy may be emerged. Disclosures: No relevant conflicts of interest to declare.

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