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Induction of functional MT1 and MT2 isoforms by calcium in anaplastic thyroid carcinoma cells
Author(s) -
Liu Zhi-Min,
Chen George G.,
Shum Cathy K.Y.,
Vlantis Alexander C.,
George Cherian M.,
Koropatnick James,
Andrew van Hasselt C.
Publication year - 2007
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2007.04.049
Subject(s) - calcium , carcinogenesis , calcium in biology , mapk/erk pathway , gene isoform , chemistry , cadmium , thyroid , cancer research , cell cycle , anaplastic thyroid cancer , metallothionein , microbiology and biotechnology , cell , thyroid cancer , medicine , endocrinology , phosphorylation , biology , biochemistry , gene , organic chemistry
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.