Induction of functional MT1 and MT2 isoforms by calcium in anaplastic thyroid carcinoma cells

Metallothionein (MT) expression in carcinogenesis of thyrocytes is unknown. We demonstrated that cadmium induced transcription of all functional MT-1 and MT-2 isoforms and promoted the cell cycle from the G1 to the S phase in thyroid cancer cells, which can be suppressed by the ERK inhibitor. Cadmiu...

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Bibliographic Details
Published in:FEBS letters 2007-05, Vol.581 (13), p.2465-2472
Main Authors: Liu, Zhi-Min, Chen, George G., Shum, Cathy K.Y., Vlantis, Alexander C., George Cherian, M., Koropatnick, James, Andrew van Hasselt, C.
Format: Article
Language:English
Subjects:
anaplastic thyroid carcinoma
ARO
Ca2
Cadmium
Calcium
Calcium - pharmacology
Calcium - physiology
calcium ions
calmodulin/calmodulin kinase
CaMK
Cell Cycle
Cell Line, Tumor
DNA Primers
ERK
ERK1/2
extracellular signal-regulated kinase
extracellular signal-regulated kinases 1 and 2
FBS
fetal bovine serum
Humans
metal transcription factor-1
metal-responsive elements
Metallothionein
Metallothionein - biosynthesis
Metallothionein - genetics
metallothioneins
MREs
MTF-1
MTs
Polymerase Chain Reaction
Protein Isoforms - biosynthesis
RNA, Neoplasm - genetics
SDS
sodium dodecyl sulfate
Thyroid carcinoma
Thyroid Neoplasms
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Summary:Metallothionein (MT) expression in carcinogenesis of thyrocytes is unknown. We demonstrated that cadmium induced transcription of all functional MT-1 and MT-2 isoforms and promoted the cell cycle from the G1 to the S phase in thyroid cancer cells, which can be suppressed by the ERK inhibitor. Cadmium exposure stimulated intracellular calcium and the phosphorylation of ERK1/2. Therefore, a common pathway initiated by a rapid rise in calcium and followed by calcium-mediated activation of ERK is involved in the transcriptional induction of functional MT1 and MT2 isoforms and in the progression of the cell cycle in thyroid cancer cells exposed to cadmium.
ISSN:0014-5793
1873-3468
DOI:10.1016/j.febslet.2007.04.049