Oral administration of fluoxetine alters the proliferation/apoptosis balance of lymphoma cells and up-regulates T cell immunity in tumor-bearing mice

Antidepressants have a controversial role with regard to their influence on cancer and immunity. Recently, we showed that fluoxetine administration induces an enhancement of the T-cell mediated immunity in naïve mice, resulting in the inhibition of tumor growth. Here we studied the effects of fluoxe...

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Publicado: 2011
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http://hdl.handle.net/20.500.12110/paper_00142999_v659_n2-3_p265_Frick
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spelling paper:paper_00142999_v659_n2-3_p265_Frick2023-06-08T14:36:53Z Oral administration of fluoxetine alters the proliferation/apoptosis balance of lymphoma cells and up-regulates T cell immunity in tumor-bearing mice Antidepressant Cancer Fluoxetine Immunity Serotonin caspase 3 cyclin B cyclin D3 cyclin E cycline fluoxetine gamma interferon protein BAD protein bcl 2 protein p15 protein p16 protein p17 protein p53 tumor necrosis factor alpha animal cell animal experiment animal model apoptosis article cancer inhibition CD8+ T lymphocyte cell cycle cell cycle arrest cell proliferation cellular immunity controlled study female lymphoma lymphoma cell mouse nonhuman priority journal protein expression treatment outcome tumor growth tumor immunity Administration, Oral Animals Apoptosis Cell Line, Tumor Cell Proliferation Female Fluoxetine Gene Expression Regulation, Neoplastic Lymphoma Mice Mice, Inbred BALB C Prognosis Serotonin Uptake Inhibitors T-Lymphocytes Tumor Markers, Biological Up-Regulation Antidepressants have a controversial role with regard to their influence on cancer and immunity. Recently, we showed that fluoxetine administration induces an enhancement of the T-cell mediated immunity in naïve mice, resulting in the inhibition of tumor growth. Here we studied the effects of fluoxetine on lymphoma proliferation/apoptosis and immunity in tumor bearing-mice. We found an increase of apoptotic cells (active Caspase-3+) and a decrease of proliferative cells (PCNA+) in tumors growing in fluoxetine-treated animals. In addition, differential gene expressions of cell cycle and death markers were observed. Cyclins D3, E and B were reduced in tumors from animals treated with fluoxetine, whereas the tumor suppressor p53 and the cell cycle inhibitors p15/INK4B, p16/INK4A and p27/Kip1 were increased. Besides, the expression of the antiapoptotic factor Bcl-2 and the proapoptotic factor Bad were lower and higher respectively in these animals. These changes were accompanied by increased IFN-γ and TNF-α levels as well as augmented circulating CD8+ T lymphocytes in tumor-bearing mice treated with the antidepressant. Therefore, we propose that the up-regulation of T-cell mediated antitumor immunity may be contributing to the alterations of tumor cell proliferation and apoptosis thus resulting in the inhibition of tumor progression. © 2011 Elsevier B.V. 2011 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00142999_v659_n2-3_p265_Frick http://hdl.handle.net/20.500.12110/paper_00142999_v659_n2-3_p265_Frick
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic Antidepressant
Cancer
Fluoxetine
Immunity
Serotonin
caspase 3
cyclin B
cyclin D3
cyclin E
cycline
fluoxetine
gamma interferon
protein BAD
protein bcl 2
protein p15
protein p16
protein p17
protein p53
tumor necrosis factor alpha
animal cell
animal experiment
animal model
apoptosis
article
cancer inhibition
CD8+ T lymphocyte
cell cycle
cell cycle arrest
cell proliferation
cellular immunity
controlled study
female
lymphoma
lymphoma cell
mouse
nonhuman
priority journal
protein expression
treatment outcome
tumor growth
tumor immunity
Administration, Oral
Animals
Apoptosis
Cell Line, Tumor
Cell Proliferation
Female
Fluoxetine
Gene Expression Regulation, Neoplastic
Lymphoma
Mice
Mice, Inbred BALB C
Prognosis
Serotonin Uptake Inhibitors
T-Lymphocytes
Tumor Markers, Biological
Up-Regulation
spellingShingle Antidepressant
Cancer
Fluoxetine
Immunity
Serotonin
caspase 3
cyclin B
cyclin D3
cyclin E
cycline
fluoxetine
gamma interferon
protein BAD
protein bcl 2
protein p15
protein p16
protein p17
protein p53
tumor necrosis factor alpha
animal cell
animal experiment
animal model
apoptosis
article
cancer inhibition
CD8+ T lymphocyte
cell cycle
cell cycle arrest
cell proliferation
cellular immunity
controlled study
female
lymphoma
lymphoma cell
mouse
nonhuman
priority journal
protein expression
treatment outcome
tumor growth
tumor immunity
Administration, Oral
Animals
Apoptosis
Cell Line, Tumor
Cell Proliferation
Female
Fluoxetine
Gene Expression Regulation, Neoplastic
Lymphoma
Mice
Mice, Inbred BALB C
Prognosis
Serotonin Uptake Inhibitors
T-Lymphocytes
Tumor Markers, Biological
Up-Regulation
Oral administration of fluoxetine alters the proliferation/apoptosis balance of lymphoma cells and up-regulates T cell immunity in tumor-bearing mice
topic_facet Antidepressant
Cancer
Fluoxetine
Immunity
Serotonin
caspase 3
cyclin B
cyclin D3
cyclin E
cycline
fluoxetine
gamma interferon
protein BAD
protein bcl 2
protein p15
protein p16
protein p17
protein p53
tumor necrosis factor alpha
animal cell
animal experiment
animal model
apoptosis
article
cancer inhibition
CD8+ T lymphocyte
cell cycle
cell cycle arrest
cell proliferation
cellular immunity
controlled study
female
lymphoma
lymphoma cell
mouse
nonhuman
priority journal
protein expression
treatment outcome
tumor growth
tumor immunity
Administration, Oral
Animals
Apoptosis
Cell Line, Tumor
Cell Proliferation
Female
Fluoxetine
Gene Expression Regulation, Neoplastic
Lymphoma
Mice
Mice, Inbred BALB C
Prognosis
Serotonin Uptake Inhibitors
T-Lymphocytes
Tumor Markers, Biological
Up-Regulation
description Antidepressants have a controversial role with regard to their influence on cancer and immunity. Recently, we showed that fluoxetine administration induces an enhancement of the T-cell mediated immunity in naïve mice, resulting in the inhibition of tumor growth. Here we studied the effects of fluoxetine on lymphoma proliferation/apoptosis and immunity in tumor bearing-mice. We found an increase of apoptotic cells (active Caspase-3+) and a decrease of proliferative cells (PCNA+) in tumors growing in fluoxetine-treated animals. In addition, differential gene expressions of cell cycle and death markers were observed. Cyclins D3, E and B were reduced in tumors from animals treated with fluoxetine, whereas the tumor suppressor p53 and the cell cycle inhibitors p15/INK4B, p16/INK4A and p27/Kip1 were increased. Besides, the expression of the antiapoptotic factor Bcl-2 and the proapoptotic factor Bad were lower and higher respectively in these animals. These changes were accompanied by increased IFN-γ and TNF-α levels as well as augmented circulating CD8+ T lymphocytes in tumor-bearing mice treated with the antidepressant. Therefore, we propose that the up-regulation of T-cell mediated antitumor immunity may be contributing to the alterations of tumor cell proliferation and apoptosis thus resulting in the inhibition of tumor progression. © 2011 Elsevier B.V.
title Oral administration of fluoxetine alters the proliferation/apoptosis balance of lymphoma cells and up-regulates T cell immunity in tumor-bearing mice
title_short Oral administration of fluoxetine alters the proliferation/apoptosis balance of lymphoma cells and up-regulates T cell immunity in tumor-bearing mice
title_full Oral administration of fluoxetine alters the proliferation/apoptosis balance of lymphoma cells and up-regulates T cell immunity in tumor-bearing mice
title_fullStr Oral administration of fluoxetine alters the proliferation/apoptosis balance of lymphoma cells and up-regulates T cell immunity in tumor-bearing mice
title_full_unstemmed Oral administration of fluoxetine alters the proliferation/apoptosis balance of lymphoma cells and up-regulates T cell immunity in tumor-bearing mice
title_sort oral administration of fluoxetine alters the proliferation/apoptosis balance of lymphoma cells and up-regulates t cell immunity in tumor-bearing mice
publishDate 2011
url https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00142999_v659_n2-3_p265_Frick
http://hdl.handle.net/20.500.12110/paper_00142999_v659_n2-3_p265_Frick
_version_ 1768545124651892736