Effects of Intracellular Calcium on Cell Survival and the MAPK Pathway in a Human Hormone-Dependent Leukemia Cell Line (TF-1)

A. Apáti, Judit Jánossy, Anna Brózik, M. Magócsi

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13 Citations (Scopus)

Abstract

Changes in the cytoplasmic calcium concentration ([Ca2+] i) regulate a wide variety of cellular processes. Here we demonstrate that increased [Ca2+]i was able to induce hormone-independent survival and proliferation, as well as to evoke apoptosis in human myelo-erythroid GM-CSF/IL-3 dependent leukemia cells (TF-1). Cellular responses induced by elevated [Ca2+]i depended on the duration and amplitude of the calcium-signal. Moderate or high, but transient, elevation of [Ca2+]i caused a transient, biphasic activation of ERK1/ 2 and protected cells from hormone withdrawal-induced apoptosis.1 In contrast, high and long-lasting elevation of [Ca 2+]i led to sustained activation of the ERK1/2 kinases and apoptosis of TF-1 cells. Our data suggest that a time-dependent action of the MAPK pathway works as a decision-point between cell proliferation and apoptosis.

Original languageEnglish
Pages (from-to)70-73
Number of pages4
JournalAnnals of the New York Academy of Sciences
Volume1010
DOIs
Publication statusPublished - 2003

Fingerprint

Cell Survival
Leukemia
Cells
Hormones
Apoptosis
Calcium
Cell Line
Chemical activation
Mitogen-Activated Protein Kinase 3
Interleukin-3
Cell proliferation
Granulocyte-Macrophage Colony-Stimulating Factor
Phosphotransferases
Cell Proliferation
Survival
Pathway
Activation
Elevation

Keywords

  • c-Fos
  • Cytoplasmic calcium concentration
  • ERK1/2

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

Cite this

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title = "Effects of Intracellular Calcium on Cell Survival and the MAPK Pathway in a Human Hormone-Dependent Leukemia Cell Line (TF-1)",
abstract = "Changes in the cytoplasmic calcium concentration ([Ca2+] i) regulate a wide variety of cellular processes. Here we demonstrate that increased [Ca2+]i was able to induce hormone-independent survival and proliferation, as well as to evoke apoptosis in human myelo-erythroid GM-CSF/IL-3 dependent leukemia cells (TF-1). Cellular responses induced by elevated [Ca2+]i depended on the duration and amplitude of the calcium-signal. Moderate or high, but transient, elevation of [Ca2+]i caused a transient, biphasic activation of ERK1/ 2 and protected cells from hormone withdrawal-induced apoptosis.1 In contrast, high and long-lasting elevation of [Ca 2+]i led to sustained activation of the ERK1/2 kinases and apoptosis of TF-1 cells. Our data suggest that a time-dependent action of the MAPK pathway works as a decision-point between cell proliferation and apoptosis.",
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author = "A. Ap{\'a}ti and Judit J{\'a}nossy and Anna Br{\'o}zik and M. Mag{\'o}csi",
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T1 - Effects of Intracellular Calcium on Cell Survival and the MAPK Pathway in a Human Hormone-Dependent Leukemia Cell Line (TF-1)

AU - Apáti, A.

AU - Jánossy, Judit

AU - Brózik, Anna

AU - Magócsi, M.

PY - 2003

Y1 - 2003

N2 - Changes in the cytoplasmic calcium concentration ([Ca2+] i) regulate a wide variety of cellular processes. Here we demonstrate that increased [Ca2+]i was able to induce hormone-independent survival and proliferation, as well as to evoke apoptosis in human myelo-erythroid GM-CSF/IL-3 dependent leukemia cells (TF-1). Cellular responses induced by elevated [Ca2+]i depended on the duration and amplitude of the calcium-signal. Moderate or high, but transient, elevation of [Ca2+]i caused a transient, biphasic activation of ERK1/ 2 and protected cells from hormone withdrawal-induced apoptosis.1 In contrast, high and long-lasting elevation of [Ca 2+]i led to sustained activation of the ERK1/2 kinases and apoptosis of TF-1 cells. Our data suggest that a time-dependent action of the MAPK pathway works as a decision-point between cell proliferation and apoptosis.

AB - Changes in the cytoplasmic calcium concentration ([Ca2+] i) regulate a wide variety of cellular processes. Here we demonstrate that increased [Ca2+]i was able to induce hormone-independent survival and proliferation, as well as to evoke apoptosis in human myelo-erythroid GM-CSF/IL-3 dependent leukemia cells (TF-1). Cellular responses induced by elevated [Ca2+]i depended on the duration and amplitude of the calcium-signal. Moderate or high, but transient, elevation of [Ca2+]i caused a transient, biphasic activation of ERK1/ 2 and protected cells from hormone withdrawal-induced apoptosis.1 In contrast, high and long-lasting elevation of [Ca 2+]i led to sustained activation of the ERK1/2 kinases and apoptosis of TF-1 cells. Our data suggest that a time-dependent action of the MAPK pathway works as a decision-point between cell proliferation and apoptosis.

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