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2014 ; 33
(18
): 2307-16
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Induction of epithelial-mesenchymal transition (EMT) in breast cancer cells is
calcium signal dependent
#MMPMID23686305
Davis FM
; Azimi I
; Faville RA
; Peters AA
; Jalink K
; Putney JW Jr
; Goodhill GJ
; Thompson EW
; Roberts-Thomson SJ
; Monteith GR
Oncogene
2014[May]; 33
(18
): 2307-16
PMID23686305
show ga
Signals from the tumor microenvironment trigger cancer cells to adopt an invasive
phenotype through epithelial-mesenchymal transition (EMT). Relatively little is
known regarding key signal transduction pathways that serve as cytosolic bridges
between cell surface receptors and nuclear transcription factors to induce EMT. A
better understanding of these early EMT events may identify potential targets for
the control of metastasis. One rapid intracellular signaling pathway that has not
yet been explored during EMT induction is calcium. Here we show that stimuli used
to induce EMT produce a transient increase in cytosolic calcium levels in human
breast cancer cells. Attenuation of the calcium signal by intracellular calcium
chelation significantly reduced epidermal growth factor (EGF)- and
hypoxia-induced EMT. Intracellular calcium chelation also inhibited EGF-induced
activation of signal transducer and activator of transcription 3 (STAT3), while
preserving other signal transduction pathways such as Akt and extracellular
signal-regulated kinase 1/2 (ERK1/2) phosphorylation. To identify
calcium-permeable channels that may regulate EMT induction in breast cancer
cells, we performed a targeted siRNA-based screen. We found that transient
receptor potential-melastatin-like 7 (TRPM7) channel expression regulated
EGF-induced STAT3 phosphorylation and expression of the EMT marker vimentin.
Although intracellular calcium chelation almost completely blocked the induction
of many EMT markers, including vimentin, Twist and N-cadherin, the effect of
TRPM7 silencing was specific for vimentin protein expression and STAT3
phosphorylation. These results indicate that TRPM7 is a partial regulator of EMT
in breast cancer cells, and that other calcium-permeable ion channels are also
involved in calcium-dependent EMT induction. In summary, this work establishes an
important role for the intracellular calcium signal in the induction of EMT in
human breast cancer cells. Manipulation of calcium-signaling pathways controlling
EMT induction in cancer cells may therefore be an important therapeutic strategy
for preventing metastases.
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