Extrinsic nitric oxide donor partially reverses arginine deiminase induced cell growth inhibition through NFκB and Bcl-XL

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Abstract

Arginine deiminase (ADI) is known to be an inducer of apoptosis in vitro and an anti-tumor agent in vivo in some cancers. ADI causes the enzymatic depletion of arginine which may inhibit nitric oxide (NO) synthesis. However, the effect of ADI treatment on NO synthesis has not been clearly elucidated. With the goal of understanding the role of ADI in NO synthesis, we used the Ramos human lymphoma cell line, which is known to be ADI-sensitive. After determining an optimal experimental ADI concentration (0.001 U/ml), we studied the effects of ADI treatment when combined with different concentrations of the extrinsic NO donor, sodium nitroprusside (SNP) (i.e., control, ADI only, ADI with 10 μM/ml SNP, ADI with 50 μM/ml SNP, and ADI with 100 μM/ml SNP). An MTT assay was used to assess cell survival after treatment, nitric oxide assays to determine nitrite levels and Western blot analysis to determine the expression of the NO mediators, NFκB and Bcl-X L . Interestingly, we found that the extrinsic NO donor only partially reversed ADI-induced inhibition of cell growth in a dose-dependent pattern and resulted in an induction of NFκB and Bcl-X L expression. In conclusion, we suggest that there might be an association between reversal of cell growth inhibition by extrinsic NO donor with Bcl-XL and NFκB expression in ADI-treated Ramos cell.

Original languageEnglish
Pages (from-to)277-282
Number of pages6
JournalInvestigational New Drugs
Volume26
Issue number3
DOIs
Publication statusPublished - 2008 Jun 1

Fingerprint

Nitric Oxide Donors
Growth
Nitroprusside
Nitric Oxide
arginine deiminase
Nitrites
Arginine
Lymphoma
Neoplasms
Cell Survival

Keywords

  • ADI
  • Bcl-X
  • NFκB
  • NO donor

ASJC Scopus subject areas

  • Molecular Medicine
  • Pharmacology

Cite this

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title = "Extrinsic nitric oxide donor partially reverses arginine deiminase induced cell growth inhibition through NFκB and Bcl-XL",
abstract = "Arginine deiminase (ADI) is known to be an inducer of apoptosis in vitro and an anti-tumor agent in vivo in some cancers. ADI causes the enzymatic depletion of arginine which may inhibit nitric oxide (NO) synthesis. However, the effect of ADI treatment on NO synthesis has not been clearly elucidated. With the goal of understanding the role of ADI in NO synthesis, we used the Ramos human lymphoma cell line, which is known to be ADI-sensitive. After determining an optimal experimental ADI concentration (0.001 U/ml), we studied the effects of ADI treatment when combined with different concentrations of the extrinsic NO donor, sodium nitroprusside (SNP) (i.e., control, ADI only, ADI with 10 μM/ml SNP, ADI with 50 μM/ml SNP, and ADI with 100 μM/ml SNP). An MTT assay was used to assess cell survival after treatment, nitric oxide assays to determine nitrite levels and Western blot analysis to determine the expression of the NO mediators, NFκB and Bcl-X L . Interestingly, we found that the extrinsic NO donor only partially reversed ADI-induced inhibition of cell growth in a dose-dependent pattern and resulted in an induction of NFκB and Bcl-X L expression. In conclusion, we suggest that there might be an association between reversal of cell growth inhibition by extrinsic NO donor with Bcl-XL and NFκB expression in ADI-treated Ramos cell.",
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author = "Seo, {Jae Hong} and Sung, {Hwa Jung} and Choi, {Chul Won} and Kim, {Byung Soo} and Shin, {Sang Won} and Kim, {Yeul Hong} and Min, {Bon Hong} and Kim, {Jun Suk}",
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T1 - Extrinsic nitric oxide donor partially reverses arginine deiminase induced cell growth inhibition through NFκB and Bcl-XL

AU - Seo, Jae Hong

AU - Sung, Hwa Jung

AU - Choi, Chul Won

AU - Kim, Byung Soo

AU - Shin, Sang Won

AU - Kim, Yeul Hong

AU - Min, Bon Hong

AU - Kim, Jun Suk

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N2 - Arginine deiminase (ADI) is known to be an inducer of apoptosis in vitro and an anti-tumor agent in vivo in some cancers. ADI causes the enzymatic depletion of arginine which may inhibit nitric oxide (NO) synthesis. However, the effect of ADI treatment on NO synthesis has not been clearly elucidated. With the goal of understanding the role of ADI in NO synthesis, we used the Ramos human lymphoma cell line, which is known to be ADI-sensitive. After determining an optimal experimental ADI concentration (0.001 U/ml), we studied the effects of ADI treatment when combined with different concentrations of the extrinsic NO donor, sodium nitroprusside (SNP) (i.e., control, ADI only, ADI with 10 μM/ml SNP, ADI with 50 μM/ml SNP, and ADI with 100 μM/ml SNP). An MTT assay was used to assess cell survival after treatment, nitric oxide assays to determine nitrite levels and Western blot analysis to determine the expression of the NO mediators, NFκB and Bcl-X L . Interestingly, we found that the extrinsic NO donor only partially reversed ADI-induced inhibition of cell growth in a dose-dependent pattern and resulted in an induction of NFκB and Bcl-X L expression. In conclusion, we suggest that there might be an association between reversal of cell growth inhibition by extrinsic NO donor with Bcl-XL and NFκB expression in ADI-treated Ramos cell.

AB - Arginine deiminase (ADI) is known to be an inducer of apoptosis in vitro and an anti-tumor agent in vivo in some cancers. ADI causes the enzymatic depletion of arginine which may inhibit nitric oxide (NO) synthesis. However, the effect of ADI treatment on NO synthesis has not been clearly elucidated. With the goal of understanding the role of ADI in NO synthesis, we used the Ramos human lymphoma cell line, which is known to be ADI-sensitive. After determining an optimal experimental ADI concentration (0.001 U/ml), we studied the effects of ADI treatment when combined with different concentrations of the extrinsic NO donor, sodium nitroprusside (SNP) (i.e., control, ADI only, ADI with 10 μM/ml SNP, ADI with 50 μM/ml SNP, and ADI with 100 μM/ml SNP). An MTT assay was used to assess cell survival after treatment, nitric oxide assays to determine nitrite levels and Western blot analysis to determine the expression of the NO mediators, NFκB and Bcl-X L . Interestingly, we found that the extrinsic NO donor only partially reversed ADI-induced inhibition of cell growth in a dose-dependent pattern and resulted in an induction of NFκB and Bcl-X L expression. In conclusion, we suggest that there might be an association between reversal of cell growth inhibition by extrinsic NO donor with Bcl-XL and NFκB expression in ADI-treated Ramos cell.

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