Altered expression of key cellular gene products accompanies development of resistance to nitric oxide.
Identifieur interne : 001650 ( Main/Exploration ); précédent : 001649; suivant : 001651Altered expression of key cellular gene products accompanies development of resistance to nitric oxide.
Auteurs : Miguel Aguilar-Santelises [Suède] ; Marlene Mozart ; Richard Scuderi ; Fredrik CelsingSource :
- Nitric oxide : biology and chemistry / official journal of the Nitric Oxide Society [ 1089-8603 ] ; 2006.
English descriptors
- KwdEn :
- MESH :
- chemical , pharmacology : Nitric Oxide Donors.
- chemical , physiology : Nitric Oxide.
- Apoptosis, Cell Line, Tumor, Drug Resistance, Humans, Signal Transduction.
Abstract
NALM-6 is a pre-B leukemia cell line sensitive to exogenous nitric oxide (NO), which enters into apoptosis during 24 h of exposure to low doses of the NO donors SNAP (100 microM) or DETA-NO (250 microM). By culturing NALM-6 with repeated and increasing concentrations of SNAP, we obtained a variant (NALM-6R) that retains >95% viability and does not enter into apoptosis during 24 h culture in the presence of up to 500 microM SNAP or 750 microM DETA-NO. A power blot screen performed with 277 antibodies on cell lysates from NALM-6 and NALM-6R cultured without NO donors served to determine the altered constitutive expression of 19 proteins in NALM-6R. Proteins affected in the less sensitive cell line NALM6-R are involved in the regulation of apoptosis, the cell cycle, cell interactions, signal transduction, cell morphology, and cell motility. This model shows that repeated exposure of tumor cells to NO may either select NO-resistant cells or contribute to NO-sensitive conversion into NO-resistant cells. The identification of the proteins that are affected during this transition may help us to define the mechanisms that are involved in cell resistance to NO-cytotoxicity which often accompany clinical progression.
DOI: 10.1016/j.niox.2006.03.007
PubMed: 16675276
Affiliations:
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Le document en format XML
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<affiliation wicri:level="1"><nlm:affiliation>Department of Medicine, Division of Hematology, Karolinska University Hospital, Stockholm, Sweden.</nlm:affiliation>
<country xml:lang="fr">Suède</country>
<wicri:regionArea>Department of Medicine, Division of Hematology, Karolinska University Hospital, Stockholm</wicri:regionArea>
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<author><name sortKey="Mozart, Marlene" sort="Mozart, Marlene" uniqKey="Mozart M" first="Marlene" last="Mozart">Marlene Mozart</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Altered expression of key cellular gene products accompanies development of resistance to nitric oxide.</title>
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<author><name sortKey="Mozart, Marlene" sort="Mozart, Marlene" uniqKey="Mozart M" first="Marlene" last="Mozart">Marlene Mozart</name>
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<author><name sortKey="Scuderi, Richard" sort="Scuderi, Richard" uniqKey="Scuderi R" first="Richard" last="Scuderi">Richard Scuderi</name>
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<series><title level="j">Nitric oxide : biology and chemistry / official journal of the Nitric Oxide Society</title>
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<term>Nitric Oxide (physiology)</term>
<term>Nitric Oxide Donors (pharmacology)</term>
<term>Signal Transduction</term>
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<keywords scheme="MESH" xml:lang="en"><term>Apoptosis</term>
<term>Cell Line, Tumor</term>
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<front><div type="abstract" xml:lang="en">NALM-6 is a pre-B leukemia cell line sensitive to exogenous nitric oxide (NO), which enters into apoptosis during 24 h of exposure to low doses of the NO donors SNAP (100 microM) or DETA-NO (250 microM). By culturing NALM-6 with repeated and increasing concentrations of SNAP, we obtained a variant (NALM-6R) that retains >95% viability and does not enter into apoptosis during 24 h culture in the presence of up to 500 microM SNAP or 750 microM DETA-NO. A power blot screen performed with 277 antibodies on cell lysates from NALM-6 and NALM-6R cultured without NO donors served to determine the altered constitutive expression of 19 proteins in NALM-6R. Proteins affected in the less sensitive cell line NALM6-R are involved in the regulation of apoptosis, the cell cycle, cell interactions, signal transduction, cell morphology, and cell motility. This model shows that repeated exposure of tumor cells to NO may either select NO-resistant cells or contribute to NO-sensitive conversion into NO-resistant cells. The identification of the proteins that are affected during this transition may help us to define the mechanisms that are involved in cell resistance to NO-cytotoxicity which often accompany clinical progression.</div>
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<name sortKey="Scuderi, Richard" sort="Scuderi, Richard" uniqKey="Scuderi R" first="Richard" last="Scuderi">Richard Scuderi</name>
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