Taurine-Responsive Genes Related to Signal Transduction as Identified by cDNA Microarray Analyses of HepG2 Cells

2006 ◽  
Vol 9 (1) ◽  
pp. 33-41 ◽  
Author(s):  
Sung-Hee Park ◽  
Haemi Lee ◽  
Kun Koo Park ◽  
Ha Won Kim ◽  
Taesun Park
Keyword(s):  
Signal Transduction ◽  
Cdna Microarray ◽  
Hepg2 Cells ◽  
Microarray Analyses

scholarly journals Mechanisms of benzene-induced hematotoxicity and leukemogenicity: cDNA microarray analyses using mouse bone marrow tissue.

2003 ◽  
Vol 111 (11) ◽  
pp. 1411-1420 ◽  
Author(s):  
Byung-Il Yoon ◽  
Guang-Xun Li ◽  
Kunio Kitada ◽  
Yasushi Kawasaki ◽  
Katsuhide Igarashi ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Cdna Microarray ◽  
Mouse Bone Marrow ◽  
Bone Marrow Tissue ◽  
Microarray Analyses

scholarly journals Distinct Nongenomic Signal Transduction Pathways Controlled by 17β-Estradiol Regulate DNA Synthesis and Cyclin D1 Gene Transcription in HepG2 Cells

2002 ◽  
Vol 13 (10) ◽  
pp. 3720-3729 ◽  
Author(s):  
Maria Marino ◽  
Filippo Acconcia ◽  
Francesco Bresciani ◽  
Alessandro Weisz ◽  
Anna Trentalance
Keyword(s):  
Gene Expression ◽  
Signal Transduction ◽  
Estrogen Receptor ◽  
Protein Kinase ◽  
Dna Synthesis ◽  
Gene Transcription ◽  
Hepg2 Cells ◽  
Signal Transduction Pathways ◽  
Cyclin D ◽  
17Β Estradiol

Estrogens induce cell proliferation in target tissues by stimulating progression through the G1 phase of the cell cycle. Activation of cyclin D1 gene expression is a critical feature of this hormonal action. The existence of rapid/nongenomic estradiol-regulated protein kinase C (PKC-α) and extracellular signal-regulated kinase (ERK) signal transduction pathways, their cross talk, and role played in DNA synthesis and cyclin D1 gene transcription have been studied herein in human hepatoma HepG2 cells. 17β-Estradiol was found to rapidly activate PKC-α translocation and ERK-2/mitogen-activated protein kinase phosphorylation in this cell line. These actions were independent of each other, preceding the increase of thymidine incorporation into DNA and cyclin D1expression, and did not involve DNA binding by estrogen receptor. The results obtained with specific inhibitors indicated that PKC-α pathway is necessary to mediate the estradiol-induced G1-S progression of HepG2 cells, but it does not exert any effect(s) on cyclin D1 gene expression. On the contrary, ERK-2 cascade was strongly involved in both G1-S progression and cyclin D1gene transcription. Deletion of its activating protein-1 responsive element motif resulted in attenuation of cyclin D1 promoter responsiveness to estrogen. These results indicate that estrogen-induced cyclin D1 transcription can occur in HepG2 cells independently of the transcriptional activity of estrogen receptor, sustaining the pivotal role played by nongenomic pathways of estrogen action in hormone-induced proliferation.

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