Ferritin Gene Expression in Health and Malignancy

Pathobiology ◽  
1992 ◽  
Vol 60 (1) ◽  
pp. 10-18 ◽  
Author(s):  
A.B. Bomford ◽  
H.N. Munro
Keyword(s):  
Gene Expression ◽  
Ferritin Gene

Transforming growth factor β1 selectively regulates ferritin gene expression in malignant H-ras-transformed fibrosarcoma cell lines

2000 ◽  
Vol 78 (4) ◽  
pp. 527-535 ◽  
Author(s):  
James Lo ◽  
Robert AR Hurta
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Growth Factor ◽  
Malignant Transformation ◽  
Cell Lines ◽  
Transforming Growth Factor ◽  
Malignant Potential ◽  
Transformed Cells ◽  
Protein Synthesis Inhibitor ◽  
Ferritin Gene

Transforming growth factor β1 is an important growth regulator in many cell types, usually exerting a negative effect on cellular growth. Inhibition of DNA synthesis and cell proliferation is frequently lost during malignant transformation, and in some cases, tumor cell proliferation is actually stimulated by TGF-β1. The present study demonstrates a novel link between alterations in TGF-β1 regulation during malignant conversion, and the expression of ferritin, an important activity involved in a number of biological functions including iron homeostasis and cell-growth control. A series of H-ras-transformed mouse 10 T 1/2 cell lines, exhibiting increasing malignant potential, was investigated for possible TGF-β1-mediated changes in ferritin gene expression. Selective induction of gene expression was observed, since only H-ras-transformed cells with malignant potential exhibited marked elevations in ferritin gene expression, in particular, alterations in H-ferritin gene expression. The regulation of H-ferritin gene expression in response to TGF-β 1 did not involve alterations in transcription, but occurred through mechanisms of post-transcriptional stabilization of the H-ferritin mRNA. Additionally, evidence was obtained for a cycloheximide-sensitive regulator of H-ferritin gene expression, since the presence of this protein synthesis inhibitor increased H-ferritin message levels, and in combination with TGF-β1, cooperated in an additive manner to augment H-ferritin gene expression. These results show for the first time that TGF-β1 can regulate ferritin gene expression in malignant H-ras transformed cells, and suggest a mechanism for growth factor stimulation of malignant cells, in which early alterations in the control of H-ferritin gene expression are important.Key words: TGF-β1, ferritin gene expression, malignant transformation.

scholarly journals Post-transcriptional regulation of H-ferritin gene expression in human monocytic THP-1 cells by protein kinase C

1996 ◽  
Vol 319 (1) ◽  
pp. 185-189 ◽  
Author(s):  
Jong-Hwei S. PANG ◽  
Chia-Jung WU ◽  
Lee-Young CHAU
Keyword(s):  
Gene Expression ◽  
Protein Synthesis ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Human Fibroblasts ◽  
Leukaemic Cell ◽  
Protein Synthesis Inhibitor ◽  
Kinase C ◽  
Ferritin Gene ◽  
The Stability

The mRNA coding for H-ferritin was highly induced in human monocytic THP-1 cells following treatment with phorbol 12-myristate 13-acetate (PMA). The induction was detected at 3 h, reached maximal levels at 12 h, and was sustained for up to 48 h subsequent to PMA exposure. PMA-induced up-regulation of H-ferritin gene expression was also observed in other leukaemic cell lines, HL60 and U937, but not in non-leukaemic cell types, including human fibroblasts, endothelial cells and smooth muscle cells. The effect of PMA could be completely blocked by the protein kinase C inhibitor, H-7. Furthermore, treatment of THP-1 cells with bacterial phospholipase C also produced a marked increase in expression of H-ferritin mRNA, suggesting the activation of protein kinase C was responsible for the accumulation of mRNA. Nuclear run-off experiments demonstrated that PMA did not increase the transcriptional rate of the H-ferritin gene. In contrast, the half-life of the H-ferritin mRNA measured in the presence of actinomycin D was greatly prolonged in PMA-treated cells. The induction of H-ferritin mRNA by PMA required no protein synthesis. Conversely, treatment of THP-1 cells with protein synthesis inhibitor, cycloheximide, resulted in a 4–5-fold increase in H-ferritin mRNA. The increase in the stability of the H-ferritin mRNA was also observed in cells treated with cycloheximide. Taken together, these results suggest that the stability of H-ferritin mRNA in THP-1 is subjected to regulation via a protein kinase C-mediated phosphorylation on existing putative protein factor(s).

scholarly journals Iron storage capacities and associated ferritin gene expression among marine diatoms

2018 ◽  
Vol 63 (4) ◽  
pp. 1677-1691 ◽  
Author(s):  
Natalie R. Cohen ◽  
Elizabeth Mann ◽  
Brooke Stemple ◽  
Carly M. Moreno ◽  
Sara Rauschenberg ◽  
...  
Keyword(s):  
Gene Expression ◽  
Marine Diatoms ◽  
Iron Storage ◽  
Ferritin Gene

scholarly journals Genotypic Variation in Spatial Distribution of Fe in Rice Grains in Relation to Phytic Acid Content and Ferritin Gene Expression

Rice Science ◽  
2020 ◽  
Vol 27 (3) ◽  
pp. 227-236
Author(s):  
Anurag Mishra ◽  
Md. Shamim ◽  
Md. Wasim Siddiqui ◽  
Akanksha Singh ◽  
Deepti Srivastava ◽  
...  
Keyword(s):  
Gene Expression ◽  
Spatial Distribution ◽  
Phytic Acid ◽  
Acid Content ◽  
Genotypic Variation ◽  
Phytic Acid Content ◽  
Rice Grains ◽  
Ferritin Gene
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